Evidence map›Paper›PMID 35192423›Full record

ReviewCell cycle (Georgetown, Tex.)2022

Molecular mechanisms for ABCA1-mediated cholesterol efflux.

Lei Chen, Zhen-Wang Zhao, Peng-Hui Zeng, Ying-Jie Zhou, Wen-Jun Yin

Open access · greenAbstract readReview
In one paragraph

Review in Cell cycle (Georgetown, Tex.), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 1 pooled it
22.0field-weighted citation impact, top 1% 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

84 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.

  1. Pooled it
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  5. L-cell-specificActa pharmaceutica Sinica. B · 2026
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  13. medRxiv : the preprint server for health sciences · 2026
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  19. Jiangzhi ruanmai recipe alleviates atherosclerosis in ApoEFrontiers in cardiovascular medicine · 2026
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24 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Lei ChenDepartment of Cardiology, The Second Affiliated Hospital of Hainan Medical University, Haikou, Hainan, China.
Zhen-Wang ZhaoInstitute of Cardiovascular Disease, Key Lab for Arteriosclerology of Hunan Province, Hunan International Scientific and Technological Cooperation Base of Arteriosclerotic Disease, Hunan Province Cooperative Innovation Center for Molecular Target New Drug Study, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Peng-Hui ZengDepartment of Clinical Laboratory, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Ying-Jie ZhouDepartment of Clinical Laboratory, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
Wen-Jun YinDepartment of Clinical Laboratory, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan, China.
University of South China · CNHainan Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The maintenance of cellular cholesterol homeostasis is essential for normal cell function and viability. Excessive cholesterol accumulation is detrimental to cells and serves as the molecular basis of many diseases, such as atherosclerosis, Alzheimer's disease, and diabetes mellitus. The peripheral cells do not have the ability to degrade cholesterol. Cholesterol efflux is therefore the only pathway to eliminate excessive cholesterol from these cells. This process is predominantly mediated by ATP-binding cassette transporter A1 (ABCA1), an integral membrane protein. ABCA1 is known to transfer intracellular free cholesterol and phospholipids to apolipoprotein A-I (apoA-I) for generating nascent high-density lipoprotein (nHDL) particles. nHDL can accept more free cholesterol from peripheral cells. Free cholesterol is then converted to cholesteryl ester by lecithin:cholesterol acyltransferase to form mature HDL. HDL-bound cholesterol enters the liver for biliary secretion and fecal excretion. Although how cholesterol is transported by ABCA1 to apoA-I remains incompletely understood, nine models have been proposed to explain this effect. In this review, we focus on the current view of the mechanisms underlying ABCA1-mediated cholesterol efflux to provide an important framework for future investigation and lipid-lowering therapy.

Indexed as

Apolipoprotein A-ILipoproteins, HDLATP Binding Cassette Transporter 1Biological TransportCholesterolCholesterol, HDLPhosphatidylcholine-Sterol O-AcyltransferaseApolipoprotein A-IATP Binding Cassette Transporter 1CholesterolCholesterol, HDLLipoproteins, HDLPhosphatidylcholine-Sterol O-AcyltransferaseABCA1apoA-IcholesterolnHDLphospholipids

Identifiers

PMID35192423
PMCPMC9103275
OpenAlexW4212900905

What OpenQuestion holds

Textmetadata
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.