The DOI matches its Crossref record; 23 of the 23 references it cites were found in a registry or an index; none of the 17 sources its claims cite is checked for support yet.
Macrophage Sortilin Promotes LDL Uptake, Foam Cell Formation, and Atherosclerosis
Open accessAbstract
Rationale: Noncoding gene variants at the SORT1 locus are strongly associated with low-density lipoprotein cholesterol (LDL-C) levels, as well as with coronary artery disease. SORT1 encodes a protein called sortilin, and hepatic sortilin modulates LDL metabolism by targeting apolipoprotein B–containing lipoproteins to the lysosome. Sortilin is also expressed in macrophages, but its role in macrophage uptake of LDL and in atherosclerosis independent of plasma LDL-C levels is unknown. Objective: To determine the effect of macrophage sortilin expression on LDL uptake, foam cell formation, and atherosclerosis. Methods and Results: We crossed Sort1 −/− mice onto a humanized Apobec1 −/− ; hAPOB transgenic background and determined that Sort1 deficiency on this background had no effect on plasma LDL-C levels but dramatically reduced atherosclerosis in the aorta and aortic root. To test whether this effect was a result of macrophage sortilin deficiency, we transplanted Sort1 −/− ;LDLR −/− or Sort1 +/+ ;LDLR −/− bone marrow into Ldlr −/− mice and observed a similar reduction in atherosclerosis in mice lacking hematopoetic sortilin without an effect on plasma LDL-C levels. In an effort to determine the mechanism by which hematopoetic sortilin deficiency reduced atherosclerosis, we found no effect of sortilin deficiency on macrophage recruitment or lipopolysaccharide-induced cytokine release in vivo. In contrast, sortilin-deficient macrophages had significantly reduced uptake of native LDL ex vivo and reduced foam cell formation in vivo, whereas sortilin overexpression in macrophages resulted in increased LDL uptake and foam cell formation. Conclusions: Macrophage sortilin deficiency protects against atherosclerosis by reducing macrophage uptake of LDL. Sortilin-mediated uptake of native LDL into macrophages may be an important mechanism of foam cell formation and contributor to atherosclerosis development.
Overview
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Written from the paper’s full text.
TL;DR
Macrophage sortilin promotes native LDL uptake, foam cell formation, and atherosclerosis in mouse models, independent of plasma LDL-C levels. Sort1 deficiency in hematopoietic cells reduces atherosclerosis, whereas sortilin overexpression increases macrophage LDL uptake.
Key findings
- Total-body Sort1 deficiency on the Apobec1−/−; hAPOB Tg background did not change plasma LDL-C but reduced atherosclerosis: 68% reduction in en face aorta lesion area (P<0.0001) and 87% reduction in aortic root lesion area (P<0.0001).
- Hematopoietic Sort1 deficiency after bone marrow transplantation into Ldlr−/− mice also reduced atherosclerosis without affecting plasma LDL-C: 69% reduction in en face aortic lesion area (P<0.00001) and 34% reduction in aortic root lesion area (P<0.01).
- Sortilin-deficient macrophages had reduced foam cell formation: 28% lower total cellular cholesterol, 25% lower free cholesterol, and 32% lower cholesteryl ester (P<0.05); in vivo foam cells showed a 33% reduction in cellular cholesterol (P<0.05).
- Sortilin deficiency reduced 125I-LDL uptake by 48% in thioglycollate-elicited macrophages and 33% in bone marrow-derived macrophages (P<0.05 for both), by 39% in the absence of LDLR (P<0.05), and by 38% with cytochalasin D (P<0.05); Sort1 overexpression in J774 macrophages increased LDL uptake by 29% (P<0.05). No effect was found on thioglycollate-elicited monocyte recruitment or LPS-induced cytokine release in vivo.
Methods
- Atherosclerosis studies used Sort1−/− mice crossed onto the Apobec1−/−; hAPOB Tg background, fed a western-type diet for 18 weeks, with lesion area assessed en face and in aortic roots.
- Bone marrow from Sort1−/−;LDLR−/− or Sort1+/+;LDLR−/− donors was transplanted into irradiated Ldlr−/− recipients; after 6 weeks, mice received western diet for 18 weeks before atherosclerosis assessment.
- Macrophage studies used thioglycollate-elicited peritoneal macrophages and bone marrow-derived macrophages, with 125I-LDL uptake/degradation, Oil Red O staining, cholesterol measurements, and lentiviral Sort1 overexpression in J774 cells; statistics used 2-tailed paired Student’s t test and 1-way ANOVA with Bonferroni correction for the LPS experiment.
Limitations
- The paper does not include a formal limitations section. It states that the mechanisms of LDL-induced macrophage Sort1 upregulation require further exploration.
- Evident from the text: all causal data are from mouse atherosclerosis models and ex vivo mouse macrophages; bone marrow transplantation implicates hematopoietic cells but does not isolate macrophages from other hematopoietic cell types.
- Evident from the text: no human interventional or macrophage-specific in vivo data are presented, and the authors note mechanistic differences from another study using a different mouse model and LDL-labeling approach.
Model-written summary. Check it against the paper before relying on it.
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Cites
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Claims the paper makes
0 of 17 cited sources checked · 0 supported · 0 flagged
- Findingown data
Sort1 deficiency reduced LDL uptake by 39% in bone marrow derived macrophages lacking the LDL receptor.
“Sort1 deficiency was associated with a 39% percent reduction in LDL uptake in the absence of the LDLR (P<0.05; Figure 4f).”
Quote in the paperSubstantial claim - Findingown data
Sort1 deficiency had no effect on thioglycollate-elicited macrophage counts in vivo.
“There was no difference in macrophage counts between Sort1+/+ and Sort −/− mice (Online Figure IIa).”
Quote in the paperNot a substantial claim - Findingown data
Sort1-deficient macrophages had a 28% reduction in total cellular cholesterol after LDL incubation.
“Sort1 deficient macrophages had a significant 28% reduction in total cellular cholesterol”
Quote in the paperSubstantial claim - Findingown data
Sort1 overexpression in J774 macrophages led to a 29% increase in LDL uptake.
“Sort1 overexpression in macrophages led to a 29% increase in LDL uptake (P< 0.05; Figure 4e).”
Quote in the paperSubstantial claim - Findingown data
Sort1-deficient macrophages had a 25% reduction in free cholesterol after LDL incubation.
“a 25% reduction in free cholesterol”
Quote in the paperSubstantial claim
- Findingown data
In vivo, macrophages from Sort1−/−;Apobec−/−;hApob Tg mice fed a western-type diet for 18 weeks had a 33% reduction in cellular cholesterol content compared with macrophages from Sort1+/+ mice.
“and a significant 33% reduction in cellular cholesterol content compared to macrophages isolated from Sort1+/+ mice (P<0.05; Figure 3e–f).”
Quote in the paperSubstantial claim - Findingown data
Sort1−/−;Ldlr−/− macrophages had reduced Oil Red O staining after LDL incubation compared with control macrophages.
“Sort1−/−;Ldlr−/− macrophages had a clear and consistent reduction in Oil Red O staining (Figure 3a).”
Quote in the paperSubstantial claim - Findingown data
Sort1 mRNA abundance increased over 400-fold in wild-type thioglycollate-elicited peritoneal macrophages incubated with high concentrations of LDL.
“Sort1 mRNA abundance increased over 400-fold with LDL incubation (P <0.05; Figure 4a)”
Quote in the paperSubstantial claim - Findingown data
Sort1 deficiency reduced 125I-LDL uptake by 48% in thioglycollate-elicited peritoneal macrophages.
“Sort1 deficiency was associated with a 48% and 33% percent reduction in LDL uptake, respectively (P <0.05 for both; Figure 4c–d).”
Quote in the paperSubstantial claim - Findingown data
Hematopoietic sortilin deficiency, produced by transplanting Sort1−/−;Ldlr−/− bone marrow into Ldlr−/− mice, reduced en face aortic lesion area by 69% compared with Sort1+/+;Ldlr−/− bone marrow after 18 weeks on a western-type diet.
“Mice transplanted with Sort1−/−;Ldlr−/− bone marrow had a 69% reduction in en face aortic lesion area (P<0.00001)”
Quote in the paperSubstantial claim - Findingown data
Sortilin protein increased significantly in wild-type macrophages with LDL incubation.
“sortilin protein also increased significantly with LDL incubation (Figure 4b).”
Quote in the paperNot a substantial claim - Findingown data
Sort1 deficiency reduced 125I-LDL uptake by 33% in bone marrow derived macrophages.
“Sort1 deficiency was associated with a 48% and 33% percent reduction in LDL uptake, respectively (P <0.05 for both; Figure 4c–d).”
Quote in the paperSubstantial claim - Findingown data
Sort1-deficient macrophages had a 32% reduction in cholesteryl ester after LDL incubation.
“and a 32% reduction in cholesteryl ester (P<0.05; Figure 3b–d).”
Quote in the paperSubstantial claim - Findingown data
Total body Sort1 deficiency on the Apobec1−/−; hAPOB Tg background had no effect on plasma total and LDL cholesterol levels after 18 weeks on a western-type diet.
“On this genetic background, total and LDL cholesterol levels were not different in Sort1−/− mice compared with Sort1+/+ mice (Figure 1a,b).”
Quote in the paperSubstantial claim - Findingown data
Total body Sort1 deficiency on the Apobec1−/−; hAPOB Tg background reduced en face aorta lesion area by 68% compared with Sort1+/+ mice after 18 weeks on a western-type diet.
“After 18 weeks on diet, Sort1−/− mice had a 68% reduction in en face aorta lesion area (P <0.0001 Figure 1c,d)”
Quote in the paperSubstantial claim - Findingown data
Total body Sort1 deficiency on the Apobec1−/−; hAPOB Tg background reduced aortic root lesion area by 87% compared with Sort1+/+ mice after 18 weeks on a western-type diet.
“and an 87% reduction in aortic root lesion area (P <0.0001 Figure 1e,f) compared with Sort1+/+ mice”
Quote in the paperSubstantial claim - Findingown data
Hematopoietic sortilin deficiency had no effect on plasma LDL-C levels.
“without an effect on plasma LDL-C levels”
Quote in the paperSubstantial claim - Findingown data
Sort1 deficiency reduced LDL uptake by 38% in bone marrow derived macrophages in the presence of cytochalasin D.
“Sort1 deficiency was associated with a 38% reduction in LDL uptake in the presence of cytochalasin D (P< 0.05; Figure 4f).”
Quote in the paperSubstantial claim - Findingown data
In vivo, macrophages from Sort1−/−;Apobec−/−;hApob Tg mice fed a western-type diet for 18 weeks had reduced Oil Red O staining compared with macrophages from Sort1+/+ mice.
“macrophages isolated from Sort1−/− mice had reduced Oil Red O staining”
Quote in the paperSubstantial claim - Findingown data
Sort1 deficiency had no effect on LPS-induced cytokine levels in vivo.
“Cytokine levels post LPS injection were found to be similar between Sort1−/− and Sort1 +/+ (Online Figure IIb,c).”
Quote in the paperNot a substantial claim - Findingown data
Hematopoietic sortilin deficiency reduced aortic root lesion area by 34% compared with control bone marrow after 18 weeks on a western-type diet.
“and a 34% reduction in aortic root lesion area (P < 0.01) compared to mice transplanted with Sort1+/+;Ldlr−/− bone marrow”
Quote in the paperSubstantial claim - Interpretationown data
Macrophage sortilin deficiency protects against atherosclerosis by reducing macrophage uptake of LDL.
“Macrophage sortilin deficiency protects against atherosclerosis by reducing macrophage uptake of LDL.”
Quote in the paperSubstantial claim- Rests on an assumption: Thioglycollate-elicited peritoneal macrophages and bone-marrow-derived macrophages are representative of arterial macrophages for LDL uptake and foam cell formation.
- Premisecitation
Sortilin is expressed in macrophages.
“Sortilin is also expressed in macrophages, but little is known about its function in this cell type or its relationship to atherosclerosis.14, 15”
Quote in the paperSubstantial claim0 of 2 sources checked- cites [14] Wahe A Kasmapour B Schmaderer C Liebl D Sandhoff K Nykjaer A Griffiths G Gutierrez MG Golgi-to-phagosome transport of acid sphingomyelinase and prosaposin is mediated by sortilin Journal of cell science 2010 123 2502 2511 20571055
- cites [15] Wong I Liao H Bai X Zaknic A Zhong J Guan Y Li HY Wang YJ Zhou XF Probdnf inhibits infiltration of ed1+ macrophages after spinal cord injury Brain, behavior, and immunity 2010 24 585 597 20083190
- Interpretationown data
Macrophage sortilin promotes atherosclerosis independent of plasma LDL-C levels.
“we show here that macrophage sortilin promotes macrophage LDL uptake, foam cell formation, and atherosclerosis independent of plasma LDL-C levels.”
Quote in the paperSubstantial claim - Interpretationown data
Macrophage sortilin promotes atherosclerosis.
“we conclude that macrophage sortilin promotes LDL uptake, foam cell formation, and atherosclerosis”
Quote in the paperSubstantial claim - Interpretationown data
Increasing concentrations of extracellular LDL cause upregulation of macrophage Sort1 mRNA and protein.
“We also found that increasing concentrations of extracellular LDL causes an upregulation of macrophage Sort1 mRNA and protein.”
Quote in the paperNot a substantial claim - Interpretationown data
Macrophage sortilin promotes foam cell formation.
“we conclude that macrophage sortilin promotes LDL uptake, foam cell formation, and atherosclerosis”
Quote in the paperSubstantial claim- Rests on an assumption: Thioglycollate-elicited peritoneal macrophages and bone-marrow-derived macrophages are representative of arterial macrophages for LDL uptake and foam cell formation.
- Interpretationown data
Macrophage sortilin promotes LDL uptake.
“we conclude that macrophage sortilin promotes LDL uptake, foam cell formation, and atherosclerosis”
Quote in the paperSubstantial claim- Rests on an assumption: Thioglycollate-elicited peritoneal macrophages and bone-marrow-derived macrophages are representative of arterial macrophages for LDL uptake and foam cell formation.
- Probably not a substantial claim. 6
- It may state two separate claims as one. 9
Probably not a substantial claim.
PremisecitationSORT1 encodes the protein sortilin.
“The SORT1 gene, encoding the protein sortilin, appears to be the causal gene at the locus regulating LDL cholesterol levels9–11.”
Quote in the paperSubstantial claim0 of 3 sources checked- cites [9] Kjolby M Andersen OM Breiderhoff T Fjorback AW Pedersen KM Madsen P Jansen P Heeren J Willnow TE Nykjaer A Sort1, encoded by the cardiovascular risk locus 1p13.3, is a regulator of hepatic lipoprotein export Cell metabolism 2010 12 213 223 20816088
- cites [10] Strong A Ding Q Edmondson AC Millar JS Sachs KV Li X Kumaravel A Wang MY Ai D Guo L Alexander ET Nguyen D Lund-Katz S Phillips MC Morales CR Tall AR Kathiresan S Fisher EA Musunuru K Rader DJ Hepatic sortilin regulates both apolipoprotein b secretion and ldl catabolism The Journal of clinical investigation 2012 122 2807 2816 22751103 PMC3408750
- cites [11] Strong A Patel K Rader DJ Sortilin and lipoprotein metabolism: Making sense out of complexity Current opinion in lipidology 2014 25 350 357 25101658 PMC4565516
It may state two separate claims as one.
Interpretationown dataThe macrophage sortilin pathway is a novel pathway of macrophage cholesterol loading that quantitatively contributes to atherosclerosis.
“The macrophage sortilin pathway is a novel pathway of macrophage cholesterol loading that quantitatively contributes to atherosclerosis.”
Quote in the paperSubstantial claimIt may state two separate claims as one.
Interpretationown dataMacrophage sortilin is the first receptor-mediated pathway of uptake of native LDL leading to foam cell formation and promoting atherosclerosis development.
“Our data establish macrophage sortilin as the first receptor-mediated pathway of uptake of native LDL leading to foam cell formation and promoting atherosclerosis development.”
Quote in the paperSubstantial claimProbably not a substantial claim. It may state two separate claims as one.
PremisecitationNon-coding gene variants at the SORT1 locus are strongly associated with LDL-C levels and with coronary artery disease.
“non-coding genetic variants at chromosome 1p13 were reported to be significantly associated with myocardial infarction and CAD3, a finding that has been widely replicated4, 5. The same variants have also shown to be significantly associated with plasma levels of LDL cholesterol6–8.”
Quote in the paperSubstantial claim0 of 6 sources checked- cites [3] Samani NJ Erdmann J Hall AS Genomewide association analysis of coronary artery disease The New England journal of medicine 2007 357 443 453 17634449 PMC2719290
- cites [4] Kathiresan S Voight BF Purcell S Genome-wide association of early-onset myocardial infarction with single nucleotide polymorphisms and copy number variants Nature genetics 2009 41 334 341 19198609 PMC2681011
- cites [5] Willer CJ Sanna S Jackson AU Newly identified loci that influence lipid concentrations and risk of coronary artery disease Nature genetics 2008 40 161 169 18193043 PMC5206900
- cites [6] Kathiresan S Melander O Guiducci C Six new loci associated with blood low-density lipoprotein cholesterol, high-density lipoprotein cholesterol or triglycerides in humans Nature genetics 2008 40 189 197 18193044 PMC2682493
- cites [7] Musunuru K Strong A Frank-Kamenetsky M From noncoding variant to phenotype via sort1 at the 1p13 cholesterol locus Nature 2010 466 714 719 20686566 PMC3062476
- cites [8] Teslovich TM Musunuru K Smith AV Biological, clinical and population relevance of 95 loci for blood lipids Nature 2010 466 707 713 20686565 PMC3039276
It may state two separate claims as one.
PremisecitationMacrophages internalize native LDL through macropinocytosis, but LDL uptake cannot be fully accounted for by this process.
“Kruth and colleagues have shown that macrophages internalize native LDL through a process of macropinocytosis, although LDL uptake cannot be fully accounted for by this process1.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [1] Barthwal MK Anzinger JJ Xu Q Bohnacker T Wymann MP Kruth HS Fluid-phase pinocytosis of native low density lipoprotein promotes murine m-csf differentiated macrophage foam cell formation PloS one 2013 8 e58054 23536783 PMC3594233
It may state two separate claims as one.
Interpretationown dataSortilin-mediated uptake of native LDL into macrophages may be an important mechanism of foam cell formation and contributor to atherosclerosis development.
“Sortilin-mediated uptake of native LDL into macrophages may be an important mechanism of foam cell formation and contributor to atherosclerosis development.”
Quote in the paperSubstantial claimProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
PremisecitationHepatic sortilin binds LDL and promotes its cellular uptake and lysosomal degradation.
“hepatic sortilin binds LDL and promotes its cellular uptake and lysosomal degradation10.”
Quote in the paperNot a substantial claim0 of 1 sources checked- cites [10] Strong A Ding Q Edmondson AC Millar JS Sachs KV Li X Kumaravel A Wang MY Ai D Guo L Alexander ET Nguyen D Lund-Katz S Phillips MC Morales CR Tall AR Kathiresan S Fisher EA Musunuru K Rader DJ Hepatic sortilin regulates both apolipoprotein b secretion and ldl catabolism The Journal of clinical investigation 2012 122 2807 2816 22751103 PMC3408750
It may state two separate claims as one.
Interpretationown dataMacrophage sortilin deficiency reduces macrophage uptake of LDL and formation of foam cells, and this effect is independent of the LDL receptor and of macropinocytosis.
“These studies indicate that macrophage sortilin deficiency reduces macrophage uptake of LDL and formation of foam cells and this effect is independent of the LDL receptor and of macropinocytosis.”
Quote in the paperSubstantial claim- Rests on an assumption: Thioglycollate-elicited peritoneal macrophages and bone-marrow-derived macrophages are representative of arterial macrophages for LDL uptake and foam cell formation.
- Rests on an assumption: Cytochalasin D completely inhibits macropinocytosis under the experimental conditions, so residual LDL uptake is independent of macropinocytosis.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
PremisecitationSortilin is the causal gene at the SORT1 locus regulating LDL cholesterol levels.
“The SORT1 gene, encoding the protein sortilin, appears to be the causal gene at the locus regulating LDL cholesterol levels9–11.”
Quote in the paperNot a substantial claim0 of 3 sources checked- cites [9] Kjolby M Andersen OM Breiderhoff T Fjorback AW Pedersen KM Madsen P Jansen P Heeren J Willnow TE Nykjaer A Sort1, encoded by the cardiovascular risk locus 1p13.3, is a regulator of hepatic lipoprotein export Cell metabolism 2010 12 213 223 20816088
- cites [10] Strong A Ding Q Edmondson AC Millar JS Sachs KV Li X Kumaravel A Wang MY Ai D Guo L Alexander ET Nguyen D Lund-Katz S Phillips MC Morales CR Tall AR Kathiresan S Fisher EA Musunuru K Rader DJ Hepatic sortilin regulates both apolipoprotein b secretion and ldl catabolism The Journal of clinical investigation 2012 122 2807 2816 22751103 PMC3408750
- cites [11] Strong A Patel K Rader DJ Sortilin and lipoprotein metabolism: Making sense out of complexity Current opinion in lipidology 2014 25 350 357 25101658 PMC4565516
It may state two separate claims as one.
Study design and conductown dataBody, liver and spleen weights, peripheral blood counts, and hepatic Sort1 expression were similar between hematopoietic sortilin-deficient and control groups.
“Body, liver and spleen weights, plasma cholesterol, peripheral blood counts, and hepatic Sort1 expression were similar between groups (Online Figure I).”
Quote in the paperSubstantial claimProbably not a substantial claim.
Study design and conductown dataBone marrow engraftment in the transplant experiment was 74%.
“Bone marrow engraftment was 74% (Online Figure Ia).”
Quote in the paperSubstantial claimIt may state two separate claims as one.
PremisecitationGene deletion of SRA or CD36 does not reduce foam cell formation or atherosclerosis in mice.
“Gene deletion of known receptors of modified LDL, such as scavenger receptor A (SRA) and CD36, do not reduce foam cell formation or the development of atherosclerosis in mice2.”
Quote in the paperSubstantial claim0 of 1 sources checked- cites [2] Steinberg D The ldl modification hypothesis of atherogenesis: An update Journal of lipid research 2009 50 Suppl S376 381 19011257 PMC2674707
Probably not a substantial claim. The paper may give no reason why it holds.
Premisenone givenHepatic sortilin modulates LDL metabolism by targeting apoB-containing lipoproteins to the lysosome.
“hepatic sortilin modulates LDL metabolism by targeting apoB-containing lipoproteins to the lysosome.”
Quote in the paperNot a substantial claim
The paper relies on this without support.
Thioglycollate-elicited peritoneal macrophages and bone-marrow-derived macrophages are representative of arterial macrophages for LDL uptake and foam cell formation.
“For studies of macrophage LDL uptake, both thioglycollate-elicited peritoneal macrophages and bone-marrow derived macrophages were used.”
The paper relies on this without support.
Cytochalasin D completely inhibits macropinocytosis under the experimental conditions, so residual LDL uptake is independent of macropinocytosis.
“LDL uptake studies were performed in bone marrow derived macrophages in the presence of cytochalasin D, a potent inhibitor of actin polymerization and macropinocytosis.”
The paper relies on this without support.
LPS-induced cytokine release in vivo is a valid measure of the inflammatory pathways that contribute to atherosclerosis in this model.
“To determine if Sort1−/− mice have reduced cytokine levels, cytokine multiplexing assays were performed on Sort1−/− and Sort1+/+ mice injected with lipopolysaccharide (LPS).”
Citations
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Metadata
- Authors
- Patel, K. M., Strong, A., Tohyama, J., Jin, X., Morales, C. R., Billheimer, J., Millar, J., Kruth, H., & Rader, D. J.
- Affiliations
- National Institutes of Health (US)
- Venue
- Circulation Research
- Published
- 2015-02-27
- Volume
- 116
- Issue
- 5
- Pages
- 789-796
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- PMC
- PMC4602371
- OpenAlex
- W2039791966
- Cited by
- 194
- References
- 23
- Citations by year
- 2026: 10 · 2025: 11 · 2024: 19 · 2023: 10 · 2022: 24 · 2021: 15 · 2020: 21 · 2019: 20 · 2018: 22 · 2017: 17 · 2016: 15 · 2015: 10
- FWCI
- 9.29
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL109489)
- National Institute of General Medical Sciences (T32GM008076)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipoproteins and Cardiovascular Health
- Keywords
- sortilin, SORT1, macrophages, LDL uptake, foam cell formation, atherosclerosis, LDL receptor, apolipoprotein B, coronary artery disease, bone marrow transplantation, humanized mice, lipid metabolism
- MeSH terms
- APOBEC-1 Deaminase, Sortilin, Animals, Aortic Diseases, Bone Marrow Cells, Cytidine Deaminase, Female, Foam Cells, Lipoproteins, LDL, Cholesterol, LDL, Macrophages, Male, Mice, Transgenic, Radiation Chimera, Receptors, LDL, Macrophages, Peritoneal, Mice, Knockout, Adaptor Proteins, Vesicular Transport, Atherosclerosis, Mice, Diet, Western
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.
A language model drew the claims from the paper on 2026-11-10, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-11-10 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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