The DOI matches its Crossref record; 182 of the 184 references it cites were found in a registry or an index; 29 of the 60 sources its claims cite were checked for support.
The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk
Open accessAbstract
Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of death worldwide. Low-density lipoprotein cholesterol (LDL-C) is a well-established mediator of atherosclerosis and a key target for intervention for the primary and secondary prevention of ASCVD. However, despite substantial reduction in LDL-C, patients continue to have recurrent ASCVD events. Hypertriglyceridemia may be an important contributor of this residual risk. Observational and genetic epidemiological data strongly support a causal role of triglycerides (TGs) and the cholesterol content within triglyceride-rich lipoproteins (TGRLs) and/or remnant cholesterol (RC) in the development of ASCVD.
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Claims the paper makes
29 of 60 cited sources checked · 14 supported · 0 flagged · accuracy not yet measured
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“However, the association was attenuated after adjustment for HDL-C”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Epidemiologic Studies of TGs and Risk of CVD
What the sources say
- Partly supportedcites [72] Di Angelantonio, 2009, Major lipids, apolipoproteins, and risk of vascular disease, JAMA sourceExperimental — accuracy not yet measured
The Results (Triglyceride; page not provided) report that the triglyceride–CHD association weakened after adjustment for both HDL-C and non-HDL-C. The passage does not establish that adjustment for HDL-C alone produced the attenuation described in the claim. (LLM, conf=0.86)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“They found that the strength of an SNP's effect on TG levels correlated strongly with the magnitude of effect on CAD, after adjustment for the SNP's effects on LDL-C and HDL-C”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Genetic Studies of TGs and CVD
What the sources say
- Supportedcites [116] Do, 2013, Common variants associated with plasma triglycerides and risk for coronary artery disease, Nat Genet source
The Abstract states that the strength of a SNP’s effect on triglycerides correlates with its effect on CAD risk even after accounting for its effects on LDL-C and/or HDL-C. It also reports a strong association across 185 SNPs after adjustment for both LDL-C and HDL-C (P = 1×10−9). (LLM, conf=0.95)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“a well-known limitation of Mendelian randomization analyses is that they are susceptible to genetic pleiotropy”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Genetic Studies of TGs and CVD
What the sources say
- Supportedcites [110] Musunuru, 2016, Surprises from genetic analyses of lipid risk factors for atherosclerosis, Circ Res source
In “The Mendelian randomization study design,” the paper identifies pleiotropy as a possible shortcoming: a DNA variant may affect disease risk through mechanisms other than the biomarker being tested, undermining the causal inference. This directly supports the cited limitation. (LLM, conf=0.94)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Two large randomized controlled trials (RCTs) evaluating the efficacy of extended-release niacin vs placebo on background statin therapy in individuals with established ASCVD did not demonstrate a reduction in vascular events”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Epidemiologic Studies of TGs and Risk of CVD
What the sources say
- Partly supportedcites [18] Boden, 2011, Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy, N Engl J Med sourceExperimental — accuracy not yet measured
The Study Design and Study Population sections describe a randomized, placebo-controlled trial of 3,414 patients, and the Discussion reports no significant reduction in cardiovascular events with extended-release niacin added to intensive statin therapy. This paper establishes the result for one trial, not two: its Discussion says the other large niacin trial, HPS2-THRIVE, was still in follow-up. (LLM, conf=0.88)
- Could not verifycites [19] Crosby, 2014, Loss-of-function mutations in APOC3, triglycerides, and coronary disease, N Engl J Med sourceExperimental — accuracy not yet measured
The Discovery Cohorts and APOC3 loss-of-function results sections describe genetic associations with coronary heart disease, not niacin treatment trials. Searches for extended-release niacin, placebo, background statin therapy, and vascular events found no passage in our copy addressing the two claimed randomized trials. (LLM, conf=0.78)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Volanesorsen (previously known as ISIS-APOC-III RX ) is a second-generation ASO developed to inhibit apoCIII”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Emerging TG-Lowering Therapies
What the sources say
- Partly supportedcites [170] Gaudet, 2015, Antisense inhibition of apolipoprotein C-III in patients with hypertriglyceridemia, N Engl J Med sourceExperimental — accuracy not yet measured
The RESULTS passage describes ISIS 304801 as a second-generation antisense oligonucleotide designed to reduce APOC3 mRNA, supporting the drug class and intended target. Our copy does not identify ISIS 304801 as volanesorsen or ISIS-APOC-III RX, so it does not establish the name equivalence in the citing sentence. (LLM, conf=0.84)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes- Partly supported
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Mendelian randomization studies of variants associated with TGs are commonly affected by the pleiotropic effects of single-nucleotide polymorphisms (SNPs) on multiple metabolic pathways affecting plasma lipids, including HDL-C and LDL-C”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Genetic Studies of TGs and CVD
What the sources say
- Supportedcites [110] Musunuru, 2016, Surprises from genetic analyses of lipid risk factors for atherosclerosis, Circ Res source
In “Plasma triglyceride-rich lipoproteins as causal,” the paper says Mendelian randomization studies using triglyceride-associated SNPs are difficult to interpret because most such SNPs have pleiotropic relationships with lipids. It specifies that 87 of 94 triglyceride-associated lead SNPs were also associated with LDL-C and/or HDL-C. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites [115] Ference, 2018, Causal effect of lipids and lipoproteins on atherosclerosis: lessons from genomic studies, Cardiol Clin source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“was nonsignificant after adjustment for non-HDL-C”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Epidemiologic Studies of TGs and Risk of CVD
What the sources say
- Partly supportedcites [72] Di Angelantonio, 2009, Major lipids, apolipoproteins, and risk of vascular disease, JAMA sourceExperimental — accuracy not yet measured
The Results > Triglyceride section reports a null association between triglycerides and coronary heart disease after adjustment: HR 0.99 (95% CI, 0.94–1.05). However, that result followed adjustment for both HDL-C and non-HDL-C; the passage does not establish that adjustment for non-HDL-C alone made the association nonsignificant. (LLM, conf=0.86)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“TGs were not associated with stroke after adjustment for lipids”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Epidemiologic Studies of TGs and Risk of CVD
What the sources say
- Supportedcites [72] Di Angelantonio, 2009, Major lipids, apolipoproteins, and risk of vascular disease, JAMA source
The Methods (Statistical Analyses; page not provided) say hazard ratios were progressively adjusted for lipid measures. The Results (Triglyceride; page not provided) report adjusted triglyceride hazard ratios close to 1 for ischemic, hemorrhagic, and unclassified stroke, with confidence intervals spanning 1. This supports the claim as a finding of no statistically significant association after adjustment. (LLM, conf=0.92)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“This finding supported the notion that plasma TG levels are an independent causal risk factor for CAD”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Genetic Studies of TGs and CVD
What the sources say
- Partly supportedcites [116] Do, 2013, Common variants associated with plasma triglycerides and risk for coronary artery disease, Nat Genet sourceExperimental — accuracy not yet measured
The Abstract (page unavailable) reports that genetic effects on triglycerides correlate with CAD risk after accounting for effects on LDL-C and HDL-C, supporting the cited finding. But it concludes that triglyceride-rich lipoproteins may causally influence CAD, not that plasma triglyceride levels themselves are an independent causal risk factor. (LLM, conf=0.86)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“In the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study, addition of fenofibrate to statin therapy did not result in significant beneficial effects on CVD risk”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TG-Lowering Therapies
What the sources say
- Supportedcites [146] Ginsberg, 2010, Effects of combination lipid therapy in type 2 diabetes mellitus, N Engl J Med source
The Results > Clinical Outcomes section reports no statistically significant reduction in the primary cardiovascular outcome when fenofibrate was added to simvastatin (hazard ratio 0.92; P = 0.32). No page number is provided in our copy. (LLM, conf=0.94)
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
- The quote only partly states this claim. 4
- It may state two separate claims as one. 37
- Probably not a substantial claim. 16
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“fasting and nonfasting TG levels were associated with increased risk of coronary heart disease”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Epidemiologic Studies of TGs and Risk of CVD
What the sources say
- Partly supportedcites [72] Di Angelantonio, 2009, Major lipids, apolipoproteins, and risk of vascular disease, JAMA sourceExperimental — accuracy not yet measured
The Results > Triglyceride section reports an increased CHD risk with triglycerides after adjustment for nonlipid risk factors (HR 1.37), supporting the overall association. It does not report separate fasting and nonfasting estimates for that adjustment alone; the fasting-status estimates it does report are essentially null after further adjustment for HDL-C and non-HDL-C. (LLM, conf=0.84)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe quote only partly states this claim.
- Partly supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Mendelian randomization is essentially an RCT that has been performed by nature, because there is a random allocation of alleles to offspring at the time of conception that is unaffected by reverse causation and independent of environmental and genetic confounders”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Epidemiologic Studies of TGs and Risk of CVD
What the sources say
- Partly supportedcites [110] Musunuru, 2016, Surprises from genetic analyses of lipid risk factors for atherosclerosis, Circ Res sourceExperimental — accuracy not yet measured
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“The TG lowering is linear with a dose-dependent effect such that greater absolute reduction is seen in individuals with higher baseline TG levels”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Omega-3 fatty acids
What the sources say
- Supportedcites [148] Mozaffarian, 2011, Omega-3 fatty acids and cardiovascular disease: effects on risk factors, molecular pathways, and clinical events, J Am Coll Cardiol source
The Cardiovascular Risk Factors section states that triglyceride lowering is linearly dose-dependent and that absolute reductions are greater at higher baseline levels, while noting variable individual responses. Figure 4 also reports a larger reduction per gram of EPA+DHA in trials with higher starting triglycerides. Page numbers were not supplied in the copy. (LLM, conf=0.95)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
Every source the paper cites for this claim was checked and supports it.
In the paper
“This phenomenon occurs when the gene variant under study affects more than one pathway; thus, the observed association between the variant and disease risk may not be due to the biomarker of interest”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Genetic Studies of TGs and CVD
What the sources say
- Supportedcites [110] Musunuru, 2016, Surprises from genetic analyses of lipid risk factors for atherosclerosis, Circ Res source
The section “The Mendelian randomization study design” explicitly defines pleiotropy as a DNA variant affecting multiple mechanisms and says that its association with disease risk may therefore not be due to the biomarker in question. (LLM, conf=0.95)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
- Supported
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“LOF mutations in LPL are also associated with increased plasma TG levels and risk of ASCVD”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Genetic Studies of TGs and CVD
What the sources say
- Partly supportedcites [128] Wittrup, 1999, Lipoprotein lipase mutations, plasma lipids and lipoproteins, and risk of ischemic heart disease. A meta-analysis, Circulation sourceExperimental — accuracy not yet measured
The Plasma Triglycerides and Postheparin Plasma Lipoprotein Lipase Activity sections report that three LPL substitutions associated with reduced enzyme activity also increased triglycerides. The Risk of Ischemic Heart Disease and Discussion sections report increased risk for Gly188Glu carriers, but say any increase for Asp9Asn and Asn291Ser carriers was borderline at most. The claim overgeneralizes the cardiovascular-risk association across loss-of-function mutations. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [129] Nordestgaard, 1997, Heterozygous lipoprotein lipase deficiency: frequency in the general population, effect on plasma lipid levels, and risk of ischemic heart disease, Circulation source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“It inhibits adipose tissue lipolysis, which reduces the flux of FFAs to the liver and, therefore, leads to reduced hepatic VLDL synthesis”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Niacin
What the sources say
- Could not verifycites [167] Qin, 2011, Missense mutation in APOC3 within the C-terminal lipid binding domain of human ApoC-III results in impaired assembly and secretion of triacylglycerol-rich very low density lipoproteins: evidence that ApoC-III plays a major role in the formation of lipid precursors within the microsomal lumen, J Biol Chem sourceExperimental — accuracy not yet measured
The Discussion describes excess fatty acid influx and apoC-III’s role in hepatic VLDL assembly, but does not connect either to niacin or inhibition of adipose-tissue lipolysis. Searches for niacin, nicotinic acid, and adipose lipolysis found no passage addressing the claimed mechanism; page numbers were unavailable in our copy. (LLM, conf=0.73)
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Could not verify
None of the sources cited for this claim have been checked yet.
In the paper
“However, despite reductions in LDL-C levels with statins and newer lipid-lowering agents, substantial residual risk persists, with the majority of predicted first and recurrent ASCVD events not being averted”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“TGRL remnants have been linked to impaired coronary vasomotor function, decreased brachial artery flow-mediated dilatation, and increased carotid intima media thickness”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TGRLs and Atherosclerosis
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In pregnancy, plasma TG levels can increase two-to fourfold during the third trimester owing to physiologic hormonal changes and are generally not clinically important”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Population Distribution and Causes of Hypertriglyceridemia
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Interestingly, Mendelian randomization suggests a causal association of elevated nonfasting RC with low-grade inflammation and ischemic heart disease (IHD), whereas elevated LDL-C associates with IHD but not inflammation”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TGRL and Inflammation
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“These postprandial changes in TGs depend on baseline TG levels, fat load in the meal, and time since the last meal”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Fasting vs nonfasting measurement
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“However, the TGs are catabolized by macrophages and therefore do not accumulate in atherosclerotic plaque.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Measurement of TGs and RC
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Although lifestyle modification remains the cornerstone for management of hypertriglyceridemia, many novel drugs are in development and have shown impressive efficacy in lowering TG levels.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Abstract
Strength:boosted· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Early epidemiologic studies demonstrated that fasting TG levels independently associated with cardiovascular disease (CVD) and correlated well with nonfasting TG levels”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Fasting vs nonfasting measurement
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Other secondary causes of hypertriglyceridemia include pregnancy, hypothyroidism, chronic kidney disease, poorly controlled diabetes and/or metabolic syndrome, and medications”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Population Distribution and Causes of Hypertriglyceridemia
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These include inhibition of hepatic lipase activity and inhibition of hepatic TGRL remnant clearance”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TG Metabolism
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Collectively, these processes lead to enhanced platelet aggregation and clot formation”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TGRL and Inflammation
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Hypertriglyceridemia is frequently associated with concomitant lipoprotein alterations such as decreased high-density lipoprotein (HDL) cholesterol (HDL-C) levels and elevated levels of non-HDL-C; small, dense and total LDL particles; intermediate-density lipoprotein (IDL); and total apolipoprotein CIII (apoCIII), all of which are associated with increased ASCVD risk”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Low-density lipoprotein cholesterol (LDL-C) is a well-established mediator of atherosclerosis and a key target for intervention for the primary and secondary prevention of ASCVD.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Accordingly, several current recommendations support the use of a random, nonfasting lipid profile in clinical practice for CV risk prediction”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Fasting vs nonfasting measurement
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“At these levels, chylomicrons are usually the main carriers of TG in plasma.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Population Distribution and Causes of Hypertriglyceridemia
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Moderately elevated TG concentrations are commonly due to suboptimal lifestyle habits, including diets enriched in simple carbohydrates and/or saturated fats, excess alcohol consumption, obesity, and sedentary behavior.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Population Distribution and Causes of Hypertriglyceridemia
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thyroid hormone is an important regulator of LPL activity and elevated TG levels in hypothyroidism are due to decreased LPL activity”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Population Distribution and Causes of Hypertriglyceridemia
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“Circulating plasma apoB-containing lipoproteins penetrate the endothelial cell lining of the artery wall in susceptible regions and enter the intimal space, where they may be trapped by interaction with subendothelial proteoglycans”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Measurement of TGs and RC
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“TGRLs can readily penetrate the arterial wall and are susceptible to retention by connective tissue matrix through interaction of the positively charged residues (arginine and lysine) on apoB with the negatively charged sulfate groups of subendothelial proteoglycans, similar to LDL.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TGRLs and Atherosclerosis
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Endothelial dysfunction often precedes the development of atherosclerosis.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TGRLs and Atherosclerosis
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✗ Based: failsProbably not a substantial claim. The paper’s conclusions may not depend on it. The paper may give no reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Incomplete lipidation of apoB by MTP leads to its proteasomal degradation with subsequent decrease in VLDL production.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TG Metabolism
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Hypertriglyceridemia is a well-known cause of acute pancreatitis.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Population Distribution and Causes of Hypertriglyceridemia
Strength:boosted· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Increase in estrogen levels during the third trimester stimulates hepatic VLDL secretion and reduces the clearance of TGs by lipoprotein lipases (LPLs) in the liver and adipose tissues resulting in elevated TG levels”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Population Distribution and Causes of Hypertriglyceridemia
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Hypertriglyceridemia occurs because of increased TG production, altered processing and catabolism of TGRLs, or reduced clearance.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Population Distribution and Causes of Hypertriglyceridemia
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“It is important to note that although apoCIII is a potent inhibitor of LPL activation, recent studies have shown that it has a pleiotropic role in the regulation of TGRL metabolism independent of LPL pathways.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TG Metabolism
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“This suggests that the cholesterol content in TGRLs (e.g., RC), rather than the TGs, may be more important in atherogenesis, because it accumulates in atherosclerotic plaque and is in the causal pathway of atherosclerosis.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Measurement of TGs and RC
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“More commonly, the genetic basis for moderate to severe hypertriglyceridemia is polygenic, which can synergize with environmental factors to profoundly alter TG/VLDL production and clearance”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > ESSENTIAL POINTS
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“This notion is of particular interest because the burgeoning epidemics of obesity, metabolic syndrome, and diabetes are associated with a dramatic increase in the prevalence of hypertriglyceridemia and its potential intersection with ASCVD”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Furthermore, impairment of endothelium-dependent vasodilation and increased oxidative stress may also play a role in promoting endothelial dysfunction”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TGRLs and Atherosclerosis
Strength:hedged· not yet calibratedCausal:conditional· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The long-term clinical consequences of hepatic steatosis due to pharmacologic apoB or MTP inhibition in humans remain unclear”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TG Metabolism
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“The constitutive production and regulation of hepatic apoB plays a key role in VLDL synthesis and secretion, and safeguards against hepatic steatosis.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TG Metabolism
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Furthermore, in the insulin-resistant state, increased adipocyte lipolysis results in increased FFA flux to the liver, which also fuels the lipidation of apoB leading to increased VLDL production and de novo hepatic lipogenesis”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > ESSENTIAL POINTS
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“At this time, these direct assays to measure RC have limited clinical applicability because they do not measure all RC in the plasma and are labor intensive and costly.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Measurement of TGs and RC
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“Within macrophages, cholesterol cannot be metabolized; thus it accumulates, leading to engorged, dysfunctional foam cells.”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Measurement of TGs and RC
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes? Based: unclearIt may state two separate claims as one.
None of the sources cited for this claim have been checked yet.
In the paper
“In addition, equivocal clinical trial results of TG-lowering therapies have raised the question as to whether TGs represent a surrogate for other causal mechanisms at play for atherosclerotic disease”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Abstract
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
In the paper
“nonfasting calculated RC was associated with a stepwise increase in risk of IHD, MI, and all-cause mortality”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Epidemiologic Studies of TGs and Risk of CVD
What the sources say
- Not checked — no full text of the sourcecites [112] Varbo, 2015, Extreme nonfasting remnant cholesterol vs extreme LDL cholesterol as contributors to cardiovascular disease and all-cause mortality in 90000 individuals from the general population, Clin Chem source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesThe quote only partly states this claim.
In the paper
“The Fenofibrate Intervention and Event Lowering in Diabetes (FIELD) study with fenofibrate did not demonstrate a reduction in the rate of the composite primary outcome (CHD death and nonfatal MI) compared with placebo but was associated with a reduction in total CV events”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > TG-Lowering Therapies
What the sources say
- Not checked — no full text of the sourcecites [137] Keech, 2005, Effects of long-term fenofibrate therapy on cardiovascular events in 9795 people with type 2 diabetes mellitus (the FIELD study): randomised controlled trial, Lancet source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“TG reduction is mediated by multiple mechanisms, including increased FA catabolism by peroxisomal b-oxidation, decreased hepatic lipogenesis, and increased clearance of plasma TGs”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Omega-3 fatty acids
What the sources say
- Not checked — no full text of the sourcecites [149] Jacobson, 2012, Effects of eicosapentaenoic acid and docosahexaenoic acid on low-density lipoprotein cholesterol and other lipids: a review, J Clin Lipidol source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“It is important to note that most of these observational epidemiologic studies were done in the prestatin era”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Epidemiologic Studies of TGs and Risk of CVD
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“a pooled analysis of the Incremental Decrease in End Points Through Aggressive Lipid Lowering (IDEAL) and Treating to New Targets (TNT) trials demonstrated that increased TG levels were associated with higher risk of CVD events in statin-treated patients, although the risk was attenuated after adjustment for HDL-C and apoB-to-apoA-I ratio”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Epidemiologic Studies of TGs and Risk of CVD
What the sources say
- Not checked — no full text of the sourcecites [109] Faergeman, 2009, Plasma triglycerides and cardiovascular events in the Treating to New Targets and Incremental Decrease in End-Points through Aggressive Lipid Lowering trials of statins in patients with coronary artery disease, Am J Cardiol source
Strength:boosted· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“#30%”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Emerging TG-Lowering Therapies
What the sources say
- Not checked — no full text of the sourcecites [15] Shapiro, 2016, From lipids to inflammation: new approaches to reducing atherosclerotic risk, Circ Res source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe quote only partly states this claim.
In the paper
“In clinical trials, intramuscular injection of alipogene tiparvovec was associated with reduction in the incidence of pancreatitis and was well tolerated”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Emerging TG-Lowering Therapies
What the sources say
- Not checked — no full text of the sourcecites [172] Gaudet, 2012, Gene therapy for lipoprotein lipase deficiency, Curr Opin Lipidol source
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
In the paper
“#20% reduction in plasma TG levels with moderate to intense aerobic exercise”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Emerging TG-Lowering Therapies
What the sources say
- Not checked — no full text of the sourcecites [38] Watts, 2013, Demystifying the management of hypertriglyceridaemia, Nat Rev Cardiol source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesThe quote only partly states this claim.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“it is established that LDL is the primary causal factor in the development of atherosclerosis”
§ The Forgotten Lipids: Triglycerides, Remnant Cholesterol, and Atherosclerotic Cardiovascular Disease Risk > Emerging TG-Lowering Therapies
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✗ Based: failsProbably not a substantial claim. The paper may give no reason why it holds.
The paper relies on this without support.
Plasma triglyceride concentrations serve as a surrogate measure of triglyceride-rich lipoproteins and remnant cholesterol.
“Clinically, plasma TG concentrations serve as a surrogate measure of TGRLs and RC.”
The paper relies on this without support.
Residual confounding can limit the ability to draw causal inference from observational studies linking TGs and remnant cholesterol to ASCVD.
“However, the possibility of residual confounding limits the ability to draw causal inference from these observational studies”
The paper relies on this without support.
Elevated TG levels are closely linked to non-HDL-C with high intercorrelation between the variables.
“elevated TG levels are closely linked to non-HDL-C with high intercorrelation between the variables”
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Relatives are described as both wild-type and completely deficient
MinorThe imaging statement calls the relatives wild-type while also saying they had complete ANGPTL3 deficiency. The preceding statement attributes complete deficiency to loss-of-function mutations, so the relatives' genetic status is unclear.
“In three wild-type, first-degree relatives with complete ANGPTL deficiency, CT angiography showed no evidence of coronary atherosclerotic plaque ().”
“LOF mutations leading to complete deficiency of ANGPTL are associated with a familial combined hypolipidemia, characterized by extremely low circulating LDL-C, HDL-C, and TG levels (, ).”
Citations
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Cardiovascular Risk Reduction with Icosapent Ethyl for Hypertriglyceridemia
Bhatt, D. L., Steg, P. G., Miller, M., Brinton, E. A., Jacobson, T. A., Ketchum, S. B., Doyle, R. T., Juliano, R. A., Jiao, L., Granowitz, C., et al. (2019) · New England Journal of Medicine · doi:10.1056/nejmoa1812792 · Cited by 3,317
Sequence Variations in PCSK9, Low LDL, and Protection against Coronary Heart Disease
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Flagged first, then by citations
2 of the 184 references couldn’t be matched to a known paper.
Research works printed but not linked: 1
- Chait, 2000, Endotext
Cited by
Sorted by citations
Items 101–200 of 568
Recent advances in anti-inflammatory active components and action mechanisms of natural medicines
Wu, Z., Zhang, T., Ma, X., Guo, S., Zhou, Q., Zahoor, A., & Deng, G. (2023) · Inflammopharmacology · doi:10.1007/s10787-023-01369-9 · Cited by 25
“Then, modified LDL particles are taken up by macrophages, which contain differentiated monocytes induced by M-CSF via scavenger receptors (Sandesara et al. 2019).”
BackgroundZhang, W., Wang, L., Wang, Y., Fang, Y., Cao, R., Fang, Z., Han, D. G., Huang, X., Gu, Z., Zhang, Y., et al. (2024) · Science China Life Sciences · doi:10.1007/s11427-024-2602-7 · Cited by 22
“The pathological cascade of this process involves endothelial cell damage, leading to the accumulation of lipids, inflammatory cells, smooth muscle cells, and necrotic fragments beneath the intima, which results in the formation of atherosclerotic plaques (Li, 2023; Sandesara et al., 2019).”
Folwaczny, A., Waldmann, E., Altenhofer, J., Henze, K., & Parhofer, K. G. (2021) · Nutrients · doi:10.3390/nu13051737 · Cited by 23
The Remnant Lipoprotein Hypothesis of Diabetes-Associated Cardiovascular Disease
Bornfeldt, K. (2022) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.122.317163 · Cited by 22
Berghuis, S. A., Bos, A. F., Sauer, P. J. J., & Bocca, G. (2022) · Nutrients · doi:10.3390/nu14112269 · Cited by 22
“Data suggest that elevated triglyceride levels are an independent causal risk factor for atherosclerotic cardiovascular disease [29].”
BackgroundWang, J., Jin, R., Jin, X., Wu, Z., Zhang, H., Han, Z., Xu, Z., Liu, Y., Zhao, X., Guo, X., et al. (2023) · Journal of the American Heart Association · doi:10.1161/jaha.122.029352 · Cited by 21
Chen, Y., Li, G., Guo, X., Ouyang, N., Li, Z., Ye, N., Yu, S., Yang, H., & Sun, Y. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10153388 · Cited by 20
“Due to the negative results of high-density lipoprotein (HDL)-raising drugs (niacin, cholesteryl ester transfer protein inhibitors), regulating other lipid components to reduce the residual risk of ASCVD has become the new focus for lipid intervention [6].”
BackgroundMetabolism of Triglyceride-Rich Lipoproteins
Borén, J., & Taskinen, M. (2021) · Handbook of experimental pharmacology · doi:10.1007/164_2021_520 · Cited by 22
Zafrir, B., Khoury, R., & Saliba, W. (2023) · Journal of clinical lipidology · doi:10.1016/j.jacl.2023.03.009 · Cited by 20
Remnant cholesterol and the risk of aortic valve calcium progression: insights from the MESA study
Li, Z., Hao, Q.-Y., Zeng, Y. H., Guo, J., Li, S., Gao, J., & Yang, P. (2024) · Cardiovascular Diabetology · doi:10.1186/s12933-023-02081-2 · Cited by 20
Liu, C., Zhang, Z., Li, B., et al. (2024) · Environmental Science & Technology · doi:10.1021/acs.est.3c08610 · Cited by 20
The role of remnant cholesterol in patients with ST-segment elevation myocardial infarction
Zhou, Y., Madsen, J. M., Özbek, B. T., Køber, L., Bang, L. E., Lønborg, J. T., & Engstrøm, T. (2024) · European Journal of Preventive Cardiology · doi:10.1093/eurjpc/zwae102 · Cited by 20
Vargas‐Vázquez, A., Fermín‐Martínez, C. A., Antonio‐Villa, N. E., Fernández‐Chirino, L., Ramírez‐García, D., Dávila-López, G., Díaz-Sánchez, J. P., Aguilar-Salinas, C. A., Seiglie, J. A., & Bello‐Chavolla, O. Y. (2024) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2024.117508 · Cited by 21
Li, B., Wang, A., Wang, Y., Li, L., Li, B., Yang, Z., Zhou, X. J., Gao, Z., Tang, X., Li, Y., et al. (2020) · Journal of Diabetes · doi:10.1111/1753-0407.13076 · Cited by 20
“RC refers to the metabolic residues of triglyceride-rich lipoproteins (TGRL), that is, the metabolic residues of very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and chylomicron when not fasting, and the metabolic residues of VLDL and IDL when fasting.(20) The level of RC is highly correlat…”
BackgroundBell, T. A., Liu, M., Donner, A. J., Lee, R. G., Mullick, A. E., & Crooke, R. M. (2021) · Journal of Lipid Research · doi:10.1016/j.jlr.2021.100101 · Cited by 19
“org/lic elevated plasma LDL-C continues to be a primary and significant risk factor for ASCVD (2), plasma triglyceride (TG) has also emerged as an independent risk factor (3).”
BackgroundCao, Z., Li, S., Yang, H., Xu, C., Zhang, Y., Yang, X., Yan, T., Liu, T., & Wang, Y. (2021) · EClinicalMedicine · doi:10.1016/j.eclinm.2021.100791 · Cited by 20
“Meanwhile, increased serum cholesterol level is directly combined with the atheromatous plaque formation, developing into the stenosis or occlusion of the lumen and increasing the incidence of cardiovascular and cerebrovascular events [30].”
BackgroundLi, Y., Meng, X., Wang, Z., Lin, X., Xu, Y., Mou, J., Zhou, R., Tang, Y., Lin, C. S. K., & Li, X. (2024) · Chemical Engineering Journal · doi:10.1016/j.cej.2024.152706 · Cited by 18
Zhang, J., Liu, M., Gao, J., Tian, X.-W., Song, Y., Zhang, H., & Zhao, P. (2025) · Scientific Reports · doi:10.1038/s41598-024-84092-x · Cited by 19
Erythrocyte membrane fluidity: A novel biomarker of residual cardiovascular risk in type 2 diabetes
Bianchetti, G., CEFALO, C. M. A., Ferreri, C., Sansone, A., Vitale, M., Serantoni, C., Abeltino, A., Mezza, T., Ferraro, P. M., Spirito, M. D., et al. (2023) · European Journal of Clinical Investigation · doi:10.1111/eci.14121 · Cited by 20
“9,10 15 The REDUCE-IT (Reduction of Cardiovascular Events with Icosapent Ethyl-Intervention Trial) demonstrated that addition of 4 g/day purified eicosapentaenoic acid (icosapent ethyl) in high-risk patients, with triglyceride levels of 135–499 mg/dL and optimized statin treatment, significantly…”
MethodGómez-Delgado, F., Alcala-Diaz, J. F., Leon‐Acuña, A., López-Moreno, J., Delgado‐Lista, J., Gomez‐Marin, B., Roncero‐Ramos, I., Yubero‐Serrano, E. M., Rangel-Zúñiga, O. A., Vals‐Delgado, C., et al. (2019) · European Journal of Clinical Investigation · doi:10.1111/eci.13146 · Cited by 18
Hu, W., Zhang, P., Su, Q., Li, D., Hang, Y., Ye, X., Guan, P., Dong, J., & Lü, Y. (2020) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2020.07.009 · Cited by 18
Remnant cholesterol and long-term incidence of death in coronary artery disease patients
Drexel, H., Mader, A., Larcher, B., Festa, A., Vonbank, A., Fraunberger, P., Leiherer, A., & Saely, C. H. (2025) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2024.119048 · Cited by 17
El‐Sehrawy, A. A. M. A., Khachatryan, L., Kubaev, A., Rekha, M. M., Rab, S. O., Kaur, M., Singh, M., Srivastava, M., KADHIM, A. J., & Zwamel, A. H. (2025) · BMC Endocrine Disorders · doi:10.1186/s12902-025-01887-3 · Cited by 18
“…LDL-C is a well-established mediator of atherosclerosis, despite substantial reduction in LDL-C, patients continue to have recurrent atherosclerotic cardiovascular events, therefore, hypertriglyceridemia is suggested as an important contributor of residual risk for cardio-metabolic events [45].”
Shui, X., Chen, Z., Wen, Z., Tang, L., Tang, W., Liao, Y., Wu, Z., & Chen, L. (2022) · Angiology · doi:10.1177/00033197221080911 · Cited by 19
“Whereas, patients with presence of HTN, with DM and with initial obstructive CAD had lower ORs in comparison with those without HTN, DM, or initial obstructive CAD.”
BackgroundInfluentialYang, Y., Deng, W., Wang, Y., Li, T., Chen, Y., Long, C., Wen, Q., Wu, Y., & Chen, Q. (2022) · Frontiers in Nutrition · doi:10.3389/fnut.2022.1039056 · Cited by 20
Zheng, Z., Yuan, D., Shen, C., Zhang, Z., Ye, J., & Zhu, L. (2023) · BMC Medical Genomics · doi:10.1186/s12920-023-01531-w · Cited by 17
“Atherosclerosis is the main pathological change in ASCVD, and often causes ischaemic heart disease, ischaemic stroke, peripheral artery disease and other major diseases [1–4].”
BackgroundLi, Z., Zheng, D., Zhang, T., Ruan, S., Li, N., Yang, Y., Yang, P., & Wang, D. (2023) · Hepatology Communications · doi:10.1097/hc9.0000000000000343 · Cited by 20
“[25,26] As the central of cholesterol metabolism in the body, the liver plays a crucial role in cholesterol homeostasis; approximately 50% of cholesterol is produced by the liver.”
BackgroundThe Metabolism of Coenzyme A and Its Derivatives Plays a Crucial Role in Diseases
Xie, J., Chen, X., Zheng, M., Zhu, J., & Mao, H. (2024) · Frontiers in Bioscience-Landmark · doi:10.31083/j.fbl2904143 · Cited by 18
Jia, W., Li, Y., Wan, J., Cui, X., Lu, J., Liu, J., Li, D., Li, L., Zou, T., Ding, J., et al. (2020) · Cardiovascular Drugs and Therapy · doi:10.1007/s10557-020-06965-3 · Cited by 16
High-Fat Diet Enhances Neutrophil Adhesion in LDLR-Null Mice Via Hypercitrullination of Histone H3
Osaka, M., Deushi, M., Aoyama, J., Funakoshi, T., Ishigami, A., & Yoshida, M. (2021) · JACC Basic to Translational Science · doi:10.1016/j.jacbts.2021.04.002 · Cited by 17
Li, B., Zhou, X. J., Wang, W., Gao, Z., Yan, L., Qin, G., Tang, X., Wan, Q., Chen, L., Luo, Z., et al. (2023) · Journal of Diabetes · doi:10.1111/1753-0407.13362 · Cited by 16
“To be specific, it refers to the metabolic residues of very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and chylomicron when not fasting and the metabolic residues of VLDL and IDL when fasting.(11) It has been reported that the higher the level of RC, the greater the likelihood of developin…”
BackgroundColesterol remanente, riesgo vascular y prevención de la arteriosclerosis
Pintó, X., Fanlo‐Maresma, M., Esteve, V., Millán, J., Blanco, A., Blasco, M., Díaz-Díaz, J. L., Rodríguez, Á. D., Mangas, A., Pascual, V., et al. (2023) · Clínica e Investigación en Arteriosclerosis · doi:10.1016/j.arteri.2023.02.001 · Cited by 18
Wang, R., Gerstein, H. C., Spall, H. G. C. V., Lip, G. Y. H., Olier, I., Ortega‐Martorell, S., Thabane, L., Ye, Z., & Li, G. (2023) · European Heart Journal - Quality of Care and Clinical Outcomes · doi:10.1093/ehjqcco/qcad030 · Cited by 16
Jiang, S., Wang, Y., Wang, Z., Zhang, L., Jin, F., & Li, B. (2023) · BMC Public Health · doi:10.1186/s12889-023-16566-y · Cited by 18
“The two mainstays for management of hyperlipidemia are lifestyle changes (dietary modification, exercise, weight loss, reduction of alcohol intake) and drug treatment (statins, fibrates, niacin) [5].”
BackgroundSPPARM alpha: the Lazarus effect
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NELL-1 in Genome-Wide Association Studies across Human Diseases
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“This would result in the creation of foam cells and the growth of atherosclerotic plaque [32].”
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“Numerous epidemiological, biological, and genetic investigations have confirmed the high atherogenic effect of RC in the type 2 diabetes population [12] and a strong correlation of RC with cardiovascular endpoints [13, 14].”
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Risk factors for cardiovascular diseases in patients with vitiligo: an analysis of current evidence
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“Cholesterol in TRLs has a more direct impact on the risk of cardiovascular disease [22].”
BackgroundGao, W.-Y., Chen, P., Hsu, H., Liou, J.-W., Wu, C., Wu, M., & Yen, J.-H. (2024) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2024.116598 · Cited by 14
The effect of lipid-lowering therapy on lipid-related residual risk factors: a prospective study
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“However, despite widespread use of LDL-C-cen-tric LLT, residual “lipid-associated” cardiovascular risk remains a problem, with a considerable number of predicted ASCVD unable to be averted [4].”
BackgroundLi, J.-N., Wang, M., Tan, Y., & Wang, L.-L. (2024) · The American Journal of Chinese Medicine · doi:10.1142/s0192415x24500381 · Cited by 15
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Association Between Na, K, and Lipid Intake in Each Meal and Blood Pressure
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“Similar to elevated triglycerides [43], remnant cholesterol has been recently given prominence as an independent causal risk factor for cardiovascular disease [44].”
BackgroundAssociation between remnant cholesterol and heart failure: A prospective cohort study
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“13 Despite epidemiologic data demonstrating the association between elevations in serum triglycerides and cardiovascular disease, 14 the exact level at which risk begins to increase is unclear.”
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Association between remnant cholesterol and chronic kidney disease in Chinese hypertensive patients
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Psoriasis comorbid with atherosclerosis meets in lipid metabolism
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Nanomedicine-based drug delivery strategies for the treatment of atherosclerosis
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Remnant cholesterol and new-onset atrial fibrillation: The Atherosclerosis Risk in Communities study
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“37 Despite the significant decrease in LDL-C levels, lipoprotein(a) remains an independent risk factor for cardiovascular and cerebrovascular events.”
Lin, C.-Y., Chen, P., Hsu, H., Gao, W.-Y., Wu, M., & Yen, J.-H. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms232012485 · Cited by 14
“These clinical studies indicated that inactivation of ANGPTL3 by inhibitors effectively ameliorates plasma TGs, LDL-C and lipoproteins in dyslipidemia, and thus, ANGPTL3 inhibition shows potential benefits in patients with ASCVDs [26–28].”
BackgroundInfluentialMitochondrial Adaptive Responses to Hypertriglyceridemia and Bioactive Lipids
Alberici, L. C., & Oliveira, H. C. F. (2021) · Antioxidants and Redox Signaling · doi:10.1089/ars.2021.0180 · Cited by 12
“Other lipid sources for VLDL are FFA released from adipose tissue under the action of hormone-sensitive lipase (HSL) and de novo hepatic lipogenesis, which is often driven by overnutrition or the consumption of simple sugars (93, 95).”
Irfan, A., Haider, S. H., Nasir, A., Larik, M. O., & Naz, T. (2023) · Current Problems in Cardiology · doi:10.1016/j.cpcardiol.2023.102245 · Cited by 12
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Longitudinal changes in remnant cholesterol and the risk of cardiovascular disease
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“Although there are many risk factors influencing the progress of atherosclerosis, to date, the relationship between dyslipidemia and atherosclerosis has been well documented, suggesting that dyslipidemia is an important culprit of atherosclerosis [2].”
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The Cholesterol Paradox in Long-Livers from a Sardinia Longevity Hot Spot (Blue Zone)
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“…LDL-C levels and all-cause mortality risk in subjects over 60 years [20], the possibility of reverse causality was unlikely, as at least five epidemiological studies included in this review had excluded patients with terminal diseases and even those who died within the first year of observation.”
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“These particles can further induce endothelial dysfunction by stimulating proinflammatory cytokines ( e.g. , tumor necrosis factor-alpha, IL-1 β ), impairing endothelium-dependent vasodilation, and exacerbating oxidative stress, thereby accelerating AS initiation and progression[43].”
Hu, Y. P., Wang, X., Luo, C., Zheng, T., & Tian, G. (2023) · Lipids in Health and Disease · doi:10.1186/s12944-022-01767-y · Cited by 11
“First, the causal relationship between AIP and coronary artery Adjusted for BMI, age, smoking, DBP, SBP, AST, LDL-C, ALB, FIB, D-dimer, FDP, HbA1c, eGFR, Hb, monocytes, and neutrophils CAD coronary artery disease, BMI body mass index, DBP diastolic blood pressure, SBP systolic blood pressure, AST aspartate aminotransf…”
BackgroundInfluentialLugonja, S., Pantić, I., Alempijevic, T. M., Grbovic, V. M., Djokovic, B., Todorović, Ž., Simovic, S. M., Medović, R., Zdravkovic, N. D., & Zdravković, N. (2023) · Medicina · doi:10.3390/medicina59030554 · Cited by 13
Dong, W., Yan, S., Chen, H., Zhao, J., Zhang, Z., & Gu, W. (2023) · Journal of Diabetes · doi:10.1111/1753-0407.13498 · Cited by 10
“A large number of studies 14 – 16 have shown that RC has a stronger atherogenic effect, which can significantly increase the risk of cardiovascular events and diabetic microvascular and macrovascular complications, due to a more direct effect of cholesterol content in TRLs than triglyceride (TG).”
BackgroundWang, Q.-C., & Wang, Z.-Y. (2023) · Scientific Reports · doi:10.1038/s41598-023-49403-8 · Cited by 10
Li, B., Zhou, X. J., Liu, Y., Zhang, Y., & Mu, Y. (2023) · Journal of Atherosclerosis and Thrombosis · doi:10.5551/jat.64146 · Cited by 12
“RC refers to the metabolic residues of triglyceride-rich lipoproteins (TGRLs), that is, the metabolic residues of very-low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and chylomicron when not fasting, and the metabolic residues of VLDL and IDL when fasting 14) .”
BackgroundA significant presence in atherosclerotic cardiovascular disease: Remnant cholesterol: A review
Wang, L., Zhang, Q., Wu, Z., & Huang, X. (2024) · Medicine · doi:10.1097/md.0000000000038754 · Cited by 13
“[10] As the apolipoprotein B100 scaffold, which contains phospholipids, triglycerides, and cholesteryl esters, undergoes progressive lipification, VLDL assembly takes place within the endoplasmic reticulum of hepatocytes.”
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Remnant cholesterol, vascular risk, and prevention of atherosclerosis
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Nrf2 Signaling Pathway as a Key to Treatment for Diabetic Dyslipidemia and Atherosclerosis
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“…with CNC homology-associated protein 1 (Keap1) signaling was shown to induce the activation of the expression of NAD(P)H:quinone oxidoreductase 1 (NQO1), an antioxidant enzyme that protects cells against oxidative stress and inhibits the onset of ovarian cancer [19] and prostate cancer [20].”
BackgroundJia, Y.-P., Wang, J.-M., Lyu, J.-Q., Yang, H.-H., Miao, M.-Y., Wang, X., Wan, Z.-X., Zheng, Y., Qin, L.-Q., Li, F.-R., et al. (2024) · Journal of Lipid Research · doi:10.1016/j.jlr.2024.100653 · Cited by 10
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“Obesity, excessive alcohol consumption and prolonged inactivity can cause elevated tri-glyceride levels and accompanying lipoprotein changes, which can affect atherosclerotic cardiovascular disease [36].”
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“They are gaining attention because they not only provide insights into lipid metabolism abnormalities (31 ), but also reflect oxidative stress levels (32) and cardiovascular risk better than traditional lipid measures (33, 34, 35), and predict the left ventricular configuration ( 36).”
BackgroundAtherosclerosis, gut microbiome, and exercise in a meta-omics perspective: a literature review
Tang, H., Huang, Y., Yuan, D., & Liu, J. (2024) · PeerJ · doi:10.7717/peerj.17185 · Cited by 14
“Simultaneously, it is essential to recognize that LDL-C functions as a well-established mediator in the development of AS ( Sandesara et al., 2019 ).”
BackgroundMETHODS FOR MODELING ATHEROSCLEROSIS IN RABBITS
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A New Beginning for Triglyceride-Lowering Therapies
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Li, B., Liu, Y., Zhou, X. J., Gu, W., & Mu, Y. (2024) · Journal of Diabetes Investigation · doi:10.1111/jdi.14205 · Cited by 9
“RC, the metabolic residue of triglyceride-rich lipoprotein (TGRL), indicates the metabolism residue of very low-density lipoprotein (VLDL), intermediate-density lipoprotein (IDL), and chymotrypsin during a not empty stomach, as well as metabolic residues of VLDL and IDL during an empty stomach 9 .”
BackgroundInfluentialYu, Z., Yang, H., Shou, B., Cheng, Z., Jiang, C., Yang, Y., & Xu, J. (2024) · Scientific Reports · doi:10.1038/s41598-024-58484-y · Cited by 10
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Metadata
- Authors
- Sandesara, P. B., Virani, S. S., Fazio, S., & Shapiro, M. D.
- Affiliations
- Emory University (US)
- Michael E. DeBakey VA Medical Center (US)
- Oregon Health & Science University (US)
- Corresponding author
- Shapiro, Michael D
- Venue
- Endocrine Reviews
- Publisher
- The Endocrine Society
- Published
- 2018-10-11
- Volume
- 40
- Issue
- 2
- Pages
- 537-557
- ISSN
- 0163-769X (ISSN-L)
- 1945-7189
- PMC
- PMC6416708
- OpenAlex
- W2896008418
- Cited by
- 608
- References
- 184
- Citations by year
- 2026: 92 · 2025: 103 · 2024: 122 · 2023: 117 · 2022: 62 · 2021: 61 · 2020: 30 · 2019: 18 · 2018: 2
- FWCI
- 5.28
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Endocrine Reviews (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eCommons - AKU (Aga Khan University) (submittedVersion)
- Funders
- National Institutes of Health (5R01HL132985)
- U.S. Department of Veterans Affairs (09-028)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (K12HD043488)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- triglycerides, remnant cholesterol, triglyceride-rich lipoproteins, atherosclerotic cardiovascular disease, hypertriglyceridemia, residual cardiovascular risk, VLDL, chylomicrons, LDL cholesterol
- MeSH terms
- Cholesterol, Humans, Lipoproteins, Triglycerides, Hypertriglyceridemia, Dyslipidemias, Atherosclerosis
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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