Evidence map›Paper›PMID 36727029›Full record

ReviewFrontiers in cardiovascular medicine2022

Mechanism of homocysteine-mediated endothelial injury and its consequences for atherosclerosis.

Deqiang Yuan, Jiapeng Chu, Hao Lin, Guoqi Zhu, Jun Qian, Yunan Yu, Tongqing Yao, Fan Ping, Fei Chen, Xuebo Liu

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers, 9 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed, 9 pooled it
30.1field-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, 9 syntheses or guidelines pooled it, 121 citations in OpenAlex.

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  15. Foods (Basel, Switzerland) · 2026
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  16. ETS‑1/ETS‑2 transcription factors in CVD (Review).International journal of molecular 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

10 authors at 2 institutions in 1 country.

Deqiang YuanDepartment of Cardiology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Jiapeng ChuDepartment of Cardiology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Hao LinDepartment of Cardiology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Guoqi ZhuDepartment of Cardiology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Jun QianDepartment of Cardiology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Yunan YuDepartment of Cardiology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Tongqing YaoDepartment of Cardiology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Fan PingDepartment of Cardiology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Fei ChenDepartment of Cardiology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Xuebo LiuDepartment of Cardiology, Tongji Hospital, School of Medicine, Tongji University, Shanghai, China.
Tongji Hospital · CNTongji University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Homocysteine (Hcy) is an intermediate amino acid formed during the conversion from methionine to cysteine. When the fasting plasma Hcy level is higher than 15 μmol/L, it is considered as hyperhomocysteinemia (HHcy). The vascular endothelium is an important barrier to vascular homeostasis, and its impairment is the initiation of atherosclerosis (AS). HHcy is an important risk factor for AS, which can promote the development of AS and the occurrence of cardiovascular events, and Hcy damage to the endothelium is considered to play a very important role. However, the mechanism by which Hcy damages the endothelium is still not fully understood. This review summarizes the mechanism of Hcy-induced endothelial injury and the treatment methods to alleviate the Hcy induced endothelial dysfunction, in order to provide new thoughts for the diagnosis and treatment of Hcy-induced endothelial injury and subsequent AS-related diseases.

Indexed as

atherosclerosisendothelial cellshomocysteinehyperhomocysteinemiainflammation

Identifiers

PMID36727029
PMCPMC9884709
OpenAlexW4316664909

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.