Evidence map›Paper›PMID 32772254›Full record

ReviewCurrent atherosclerosis reports2020

CD36 in Atherosclerosis: Pathophysiological Mechanisms and Therapeutic Implications.

Kunming Tian, Yan Xu, Amirhossein Sahebkar, Suowen Xu

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Current atherosclerosis reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06230406 (Role of T-Mem GEne in the Molecular Pathogenesis of Atherosclerosis), which is not on this map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
5.5field-weighted citation impact, top 3% 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.

NCT06230406 recruitingnot on this mapstarted 2023, after this paper: background citation

Role of T-Mem GEne in the Molecular Pathogenesis of Atherosclerosis

TypeobservationalSponsorIRCCS Policlinico S. DonatoRan2023 to 2026Enrolled12ConditionsAtherosclerosisArmssurgery for artherial and/or venous diseases
3 · Its place in the literature

Who cites it

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 130 citations in OpenAlex.

  1. Effects of flavonoids on atherosclerosis in ApoEFrontiers in pharmacology · 2026
    Pooled it
  2. Article
  3. Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Article
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17 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

4 authors at 3 institutions in 2 countries.

Kunming TianDepartment of Preventive Medicine, School of Public Health, Zunyi Medical University, Zunyi, Guizhou, China. nonstandstill@163.com.
Yan XuDepartment of Preventive Medicine, School of Public Health, Zunyi Medical University, Zunyi, Guizhou, China.
Amirhossein SahebkarHalal Research Center of IRI, FDA, Tehran, Iran.
Suowen XuDepartment of Endocrinology and Metabolism, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, 230037, China. sxu1984@ustc.edu.cn.ORCID 0000-0002-5488-5217
Zunyi Medical University · CNMashhad University of Medical Sciences · IRUniversity of Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purpose of reviewAtherosclerosis is a chronic disease characterized by lipid retention and inflammation in the artery wall. The retention and oxidation of low-density lipoprotein (LDL) in sub-endothelial space play a critical role in atherosclerotic plaque formation and destabilization. Oxidized LDL (ox-LDL) and other modified LDL particles are avidly taken up by endothelial cells, smooth muscle cells, and macrophages mainly through several scavenger receptors, including CD36 which is a class B scavenger receptor and membrane glycoprotein. RECENT

findingsAnimal studies performed on CD36-deficient mice suggest that deficiency of CD36 prevents the development of atherosclerosis, though with some debate. CD36 serves as a signaling hub protein at the crossroad of inflammation, lipid metabolism, and fatty acid metabolism. In addition, the level of soluble CD36 (unattached to cells) in the circulating blood was elevated in patients with atherosclerosis and other metabolic disorders. We performed a state-of-the-art review on the structure, ligands, functions, and regulation of CD36 in the context of atherosclerosis by focusing on the pathological role of CD36 in the dysfunction of endothelial cells, smooth muscle cells, monocytes/macrophages, and platelets. Finally, we highlight therapeutic possibilities to target CD36 expression/activity in atherosclerosis.

Indexed as

AnimalsAtherosclerosisCD36 AntigensCholesterolEndothelial CellsHumansHydroxymethylglutaryl-CoA Reductase InhibitorsLipoproteins, LDLMacrophagesMiceMyocytes, Smooth MusclePlaque, AtheroscleroticPlatelet ActivationSignal TransductionCD36 AntigensCholesterolHydroxymethylglutaryl-CoA Reductase InhibitorsLipoproteins, LDLoxidized low density lipoproteinAtherosclerosisCD36Endothelial cellLipid metabolismMacrophageOxidized LDL

Identifiers

PMID32772254
OpenAlexW3048205455

What OpenQuestion holds

Texttitle and abstract
Read underepoch 390

Registered trials

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.