Evidence map›Paper›PMID 35224153›Full record

ReviewGenes & diseases2022

Pathogenesis of premature coronary artery disease: Focus on risk factors and genetic variants.

Haiming Wang, Zifan Liu, Junjie Shao, Min Jiang, Xuechun Lu, Lejian Lin, Lin Wang, Qiang Xu, Haomin Zhang, Xin Li and 3 more

Open access · diamondAbstract readReview
In one paragraph

Review in Genes & diseases, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

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  15. Current RNA strategies in treating cardiovascular diseases.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Review
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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

13 authors at 2 institutions in 1 country.

Haiming WangDepartment of Cardiovascular Medicine, Chinese PLA General Hospital & Chinese PLA Medical School, Beijing 100853, PR China.
Zifan LiuDepartment of Cardiovascular Medicine, Chinese PLA General Hospital & Chinese PLA Medical School, Beijing 100853, PR China.
Junjie ShaoThe First Clinical Medical College of Inner Mongolia Medical University, Hohhot 010059, PR China.
Min JiangDepartment of Cardiovascular Medicine, Chinese PLA General Hospital & Chinese PLA Medical School, Beijing 100853, PR China.
Xuechun LuDepartment of Hematology, The Second Medical Center of Chinese PLA General Hospital & Chinese PLA Medical School, Beijing 100853, PR China.
Lejian LinDepartment of Cardiovascular Medicine, Chinese PLA General Hospital & Chinese PLA Medical School, Beijing 100853, PR China.
Lin WangDepartment of Cardiovascular Medicine, Chinese PLA General Hospital & Chinese PLA Medical School, Beijing 100853, PR China.
Qiang XuDepartment of Cardiovascular Medicine, Chinese PLA General Hospital & Chinese PLA Medical School, Beijing 100853, PR China.
Haomin ZhangDepartment of Hematology, The Second Medical Center of Chinese PLA General Hospital & Chinese PLA Medical School, Beijing 100853, PR China.
Xin LiDepartment of Health Services, The First Medical Center of Chinese PLA General Hospital & Chinese PLA Medical School, Beijing 100853, PR China.
Jingjing ZhouDepartment of Cardiovascular Medicine, Chinese PLA General Hospital & Chinese PLA Medical School, Beijing 100853, PR China.
Yundai ChenDepartment of Cardiovascular Medicine, Chinese PLA General Hospital & Chinese PLA Medical School, Beijing 100853, PR China.
Ran ZhangDepartment of Cardiovascular Medicine, Chinese PLA General Hospital & Chinese PLA Medical School, Beijing 100853, PR China.
Chinese PLA General Hospital · CNInner Mongolia Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of premature coronary artery disease (PCAD) is dependent on both genetic predisposition and traditional risk factors. Strategies for unraveling the genetic basis of PCAD have evolved with the advent of modern technologies. Genome-wide association studies (GWASs) have identified a considerable number of common genetic variants that are associated with PCAD. Most of these genetic variants are attributable to lipid and blood pressure-related single-nucleotide polymorphisms (SNPs). The genetic variants that predispose individuals to developing PCAD may depend on race and ethnicity. Some characteristic genetic variants have been identified in Chinese populations. Although translating this genetic knowledge into clinical applications is still challenging, these genetic variants can be used for CAD phenotype identification, genetic prediction and therapy. In this article we will provide a comprehensive review of genetic variants detected by GWASs that are predicted to contribute to the development of PCAD. We will highlight recent findings regarding CAD-related genetic variants in Chinese populations and discuss the potential clinical utility of genetic variants for preventing and managing PCAD.

Indexed as

Genetic clinical applicationsGenetic variantsGenome-wide association studiesPremature coronary artery diseaseSingle-nucleotide polymorphisms

Identifiers

PMID35224153
PMCPMC8843894
OpenAlexW3105972414

What OpenQuestion holds

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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.