Evidence map›Paper›PMID 37923248›Full record

ArticleJournal of advanced research2024

Depleting LCAT Aggravates Atherosclerosis in LDLR-deficient Hamster with Reduced LDL-Cholesterol Level.

Xiao Lin, Wei Zhang, Chun Yang, Ping Ma, Kunxiang He, Gonglie Chen, Yijun Tao, Haizhao Yan, Zhao Yang, Ling Zhang and 6 more

Open access · goldAbstract read
In one paragraph

Article in Journal of advanced research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
7.0field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

13 citing papers in PubMed, 22 citations in OpenAlex.

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  7. Rodent Models for Atherosclerosis.International journal of molecular sciences · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 4 institutions in 3 countries.

Xiao LinInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, Health Science Center, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, China; Department of Biomedical Informatics, Center for Noncoding RNA Medicine, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, 38 Xueyuan Rd, Beijing 100191, China.
Wei ZhangPeking University Hepatology Institute, Peking University People's Hospital, Beijing, China.
Chun YangDepartment of General Practice, Beijing Friendship Hospital, Capital Medical University, Beijing, China.
Ping MaInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, Health Science Center, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, China.
Kunxiang HeInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, Health Science Center, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, China.
Gonglie ChenInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, Health Science Center, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, China.
Yijun TaoInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, Health Science Center, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, China.
Haizhao YanDepartment of Molecular Pathology, Graduate School of Medicine, University of Yamanashi, Chuo, Japan.
Zhao YangFaculty of Art and Science, University of Toronto, Toronto, Canada.
Ling ZhangInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, Health Science Center, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, China.
Jianglin FanDepartment of Molecular Pathology, Graduate School of Medicine, University of Yamanashi, Chuo, Japan.
Qinghua CuiDepartment of Biomedical Informatics, Center for Noncoding RNA Medicine, State Key Laboratory of Vascular Homeostasis and Remodeling, School of Basic Medical Sciences, Peking University, 38 Xueyuan Rd, Beijing 100191, China.
Wei HuangInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, Health Science Center, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, China.
George LiuInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, Health Science Center, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, China.
Xunde XianInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, Health Science Center, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, China; Beijing Key Laboratory of Cardiovascular Receptors Research, Peking University Third Hospital, Beijing, China. Electronic address: xianxunde@bjmu.edu.cn.
Yuhui WangInstitute of Cardiovascular Sciences, School of Basic Medical Sciences, Health Science Center, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, China. Electronic address: wangyuhui2009@bjmu.edu.cn.
Peking University · CNUniversity of Yamanashi · JPCapital Medical University · CNUniversity of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionLecithin cholesterol acyltransferase (LCAT) plays a crucial role in acyl-esterifying cholesterol in plasma, which is essential for reverse cholesterol transport (RCT). Previous studies indicated that its activity on both α and β lipoproteins interpret its effects on lipoproteins for many controversial investigations of atherosclerosis.

objectivesTo better understand the relationship between LCAT, diet-induced dyslipidemia and atherosclerosis, we developed a double knockout (LCAT-/-&LDLR-/-, DKO) hamster model to evaluate the specific role of LCAT independent of LDL clearance effects.

methodsPlasma triglyceride (TG), total cholesterol (TC), high-density lipoprotein-cholesterol (HDL-C), and free cholesterol (FC) levels were measured using biochemical reagent kits. FPLC was performed to analyze the components of lipoproteins. Apolipoprotein content was assessed using western blotting (WB). The hamsters were fed a high cholesterol/high fat diet (HCHFD) to induce atherosclerosis. Oil Red O staining was employed to detect plaque formation. Peritoneal macrophages were studied to investigate the effects of LCAT on cholesterol uptake and efflux.

resultsOn HCHFD, DKO hamsters exhibited significantly elevated levels of TG and FC, while HDL-C was nearly undetectable without affecting TC levels, as compared to low-density lipoprotein receptor (LDLR)-deficient (LDLR-/-, LKO) hamsters. Lipoprotein profiling revealed a marked increase in plasma chylomicron/very low-density lipoprotein (CM/VLDL) fractions, along with an unexpected reduction in LDL fraction in DKO hamsters. Furthermore, DKO hamsters displayed aggravated atherosclerotic lesions in the aorta, aortic root, and coronary artery relative to LKO hamsters, attributed to a pro-atherogenic lipoprotein profile and impaired cholesterol efflux in macrophages.

conclusionsOur study demonstrates the beneficial role of LCAT in inhibiting atherosclerotic development and highlights the distinctive lipid metabolism characteristics in hamsters with familial hypercholesterolemia.

Indexed as

AtherosclerosisCholesterol, LDLPhosphatidylcholine-Sterol O-AcyltransferaseReceptors, LDLAnimalsCholesterolCholesterol, HDLCricetinaeDiet, High-FatDisease Models, AnimalGene Knockout TechniquesMacrophages, PeritonealMaleTriglyceridesCholesterolCholesterol, HDLCholesterol, LDLPhosphatidylcholine-Sterol O-AcyltransferaseReceptors, LDLTriglyceridesAtherosclerosisCoronary diseaseLCATLDLTriglyceride

Identifiers

PMID37923248
PMCPMC11379981
OpenAlexW4388153180

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.