Triglyceride-rich lipoproteins and cardiovascular diseases
Open accessAbstract
The global prevalence of cardiovascular diseases (CVD) continues to rise steadily, making it a leading cause of mortality worldwide. Atherosclerosis (AS) serves as a primary driver of these conditions, commencing silently at an early age and culminating in adverse cardiovascular events that severely impact patients’ quality of life or lead to fatality. Dyslipidemia, particularly elevated levels of low-density lipoprotein cholesterol (LDL-C), plays a pivotal role in AS pathogenesis as an independent risk factor. Research indicates that abnormal LDL-C accumulation within arterial walls acts as a crucial trigger for atherosclerotic plaque formation. As the disease progresses, plaque accumulation may rupture or dislodge, resulting in thrombus formation and complete blood supply obstruction, ultimately causing myocardial infarction, cerebral infarction, and other common adverse cardiovascular events. Despite adequate pharmacologic therapy targeting LDL-C reduction, patients with cardiometabolic abnormalities remain at high risk for disease recurrence, highlighting the importance of addressing lipid risk factors beyond LDL-C. Recent attention has focused on the causal relationship between triglycerides, triglyceride-rich lipoproteins (TRLs), and their remnants in AS risk. Genetic, epidemiologic, and clinical studies suggest a causal relationship between TRLs and their remnants and the increased risk of AS, and this dyslipidemia may be an independent risk factor for adverse cardiovascular events. Particularly in patients with obesity, metabolic syndrome, diabetes, and chronic kidney disease, disordered TRLs and its remnants levels significantly increase the risk of atherosclerosis and cardiovascular disease development. Accumulation of over-synthesized TRLs in plasma, impaired function of enzymes involved in TRLs lipolysis, and impaired hepatic clearance of cholesterol-rich TRLs remnants can lead to arterial deposition of TRLs and its remnants, promoting foam cell formation and arterial wall inflammation. Therefore, understanding the pathogenesis of TRLs-induced AS and targeting it therapeutically could slow or impede AS progression, thereby reducing cardiovascular disease morbidity and mortality, particularly coronary atherosclerotic heart disease.
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Endothelial-bound LPL catalyzes hydrolysis of triglycerides within TRLs, releasing free fatty acids and monoacylglycerols, which induce endothelial dysfunction and local inflammation, stimulating production of proinflammatory cytokines TNF-α, IL-1β, and IL-6.
“Endothelial-bound lipoprotein lipase (LPL) catalyzes the hydrolysis of triglycerides within TRLs, releasing free fatty acids and monoacylglycerols. These lipolysis products act as bioactive mediators that induce endothelial dysfunction and local inflammation, stimulating the production of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interle”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [18]
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredThe resulting cytokine milieu promotes endothelial activation and upregulation of adhesion molecules VCAM-1 and ICAM-1, facilitating monocyte recruitment into the arterial wall.
“The resulting cytokine milieu promotes endothelial activation and upregulation of adhesion molecules, including vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1), thereby facilitating monocyte recruitment into the arterial wall [18].”
From Targeting triglycerides for cardiovascular risk reduction (2026) · cites this paper as [18]
In “TRLs promotes AS by subendothelial accumulation” (Figure 2; page unavailable), the paper says pro-inflammatory TRLs activate the endothelium to express adhesion molecules, leading to monocyte recruitment; the figure identifies VCAM-1 and ICAM-1. It does not say that the resulting cytokine milieu drives that endothelial activation: it attributes the activation directly to TRLs and their remnants. (LLM, conf=0.83)
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- Authors
- Xu, D., Xie, L., Cheng, C., Xue, F., & Sun, C.
- Affiliations
- Shandong University (CN)
- Sheng Jing Hospital (CN)
- Liaoning Cancer Hospital & Institute (CN)
- Corresponding author
- Xue, Fei
- Sun, Chaonan
- Venue
- Frontiers in Endocrinology
- Publisher
- Frontiers Media SA
- Published
- 2024-05-31
- Volume
- 15
- Pages
- 1409653-1409653
- ISSN
- 1664-2392 (ISSN-L)
- PMC
- PMC11176465
- OpenAlex
- W4399246817
- Cited by
- 73
- References
- 97
- Citations by year
- 2026: 43 · 2025: 27 · 2024: 3
- FWCI
- 5.79
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Frontiers in Endocrinology (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- China Postdoctoral Science Foundation (2023M742124)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Keywords
- triglyceride-rich lipoproteins, atherosclerosis, cardiovascular disease, dyslipidemia, LDL cholesterol, cardiovascular risk factors, foam cell formation, arterial inflammation, coronary artery disease, cardiometabolic risk, obesity, metabolic syndrome, diabetes mellitus, chronic kidney disease, lipolysis
- MeSH terms
- Animals, Cardiovascular Diseases, Humans, Lipoproteins, Risk Factors, Triglycerides, Dyslipidemias, Atherosclerosis
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