Evidence map›Paper›PMID 35134201›Full record

ArticleThe Journal of clinical endocrinology and metabolism2022

Causal Associations Between Circulating Adipokines and Cardiovascular Disease: A Mendelian Randomization Study.

Delong Chen, Yuxuan Zhang, Abuduwufuer Yidilisi, Yi Xu, Qichao Dong, Jun Jiang

Open access · hybridAbstract read
In one paragraph

Article in The Journal of clinical endocrinology and metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
10.3field-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

39 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.

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  11. The Causal Relationship between Telomere Length and Cancer Risk: A Two-Sample Mendelian Randomization.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 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

6 authors at 2 institutions in 1 country.

Delong ChenDepartment of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0002-7313-2990
Yuxuan ZhangDepartment of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0001-9407-9589
Abuduwufuer YidilisiDepartment of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0001-8733-3585
Yi XuDepartment of Cardiology, Ningbo First Hospital, Ningbo, China.ORCID 0000-0002-3814-0506
Qichao DongDepartment of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0001-9169-552X
Jun JiangDepartment of Cardiology, The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0001-6926-9516
Second Affiliated Hospital of Zhejiang University · CNNingbo First Hospital · CN

Funding

National Natural Science Foundation of China 82170332
6 · The paper itself

Abstract

contextObservational studies have suggested associations between adipokines and cardiovascular disease (CVD), but the roles of certain adipokines remain controversial, and these associations have not yet been ascertained causally.

objectiveTo investigate whether circulating adipokines causally affect the risk of CVD using 2-sample Mendelian randomization (MR).

methodsIndependent genetic variants strongly associated with adiponectin, resistin, chemerin, and retinol binding protein 4 (RBP4) were selected from public genome-wide association studies. Summary-level statistics for CVD, including coronary artery disease (CAD), myocardial infarction, atrial fibrillation (AF), heart failure (HF), and stroke and its subtypes were collected. The inverse-variance weighted and Wald ratio methods were used for the MR estimates. The MR pleiotropy residual sum and outlier, weighted median, MR-Egger, leave-one-out analysis, MR Steiger, and colocalization analyses were used in the sensitivity analysis.

resultsGenetically predicted resistin levels were positively associated with AF risk (odds ratio [OR] 1.09; 95% confidence interval [CI], 1.04-1.13; P = 4.1 × 10-5), which was attenuated to null after adjusting for blood pressure. We observed suggestive associations between higher genetically predicted chemerin levels and an increased risk of CAD (OR 1.27; 95% CI, 1.01-1.60; P = 0.040), higher genetically predicted RBP4 levels and an increased risk of HF (OR 1.14; 95% CI, 1.02-1.27; P = 0.024). There was no causal association between genetically predicted adiponectin levels and CVD risk.

conclusionsOur findings reveal the causal association between resistin and AF, probably acting through blood pressure, and suggest potential causal associations between chemerin and CAD, RBP4, and HF.

Indexed as

Atrial FibrillationCardiovascular DiseasesAdipokinesAdiponectinGenome-Wide Association StudyHumansMendelian Randomization AnalysisPolymorphism, Single NucleotideResistinRetinol-Binding Proteins, PlasmaAdipokinesAdiponectinRBP4 protein, humanResistinRetinol-Binding Proteins, Plasmaadiponectincardiovascular diseasechemerinMendelian randomizationresistinretinol binding protein 4

Identifiers

PMID35134201
PMCPMC9113792
OpenAlexW4210986406

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.