Evidence map›Paper›PMID 36864033›Full record

ArticleNature communications2023

Retinol dehydrogenase 10 reduction mediated retinol metabolism disorder promotes diabetic cardiomyopathy in male mice.

Yandi Wu, Tongsheng Huang, Xinghui Li, Conghui Shen, Honglin Ren, Haiping Wang, Teng Wu, Xinlu Fu, Shijie Deng, Ziqi Feng and 8 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
8.3field-weighted citation impact, top 2% 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

41 citing papers in PubMed, 54 citations in OpenAlex.

  1. Retinoic acid in health and disease.Signal transduction and targeted therapy · 2026
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  8. Frontiers in plant science · 2026
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  11. Review
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  16. Article
  17. Article
  18. Article
  19. Retinoic acid signaling and metabolism in heart failure.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  20. Review
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

18 authors at 2 institutions in 1 country.

Yandi Wu *Guangdong Engineering & Technology Research Center for Disease-Model Animals, Laboratory Animal Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China.ORCID 0000-0002-9380-4109
Tongsheng Huang *Guangdong Engineering & Technology Research Center for Disease-Model Animals, Laboratory Animal Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China.ORCID 0000-0002-7944-5242
Xinghui Li *Guangdong Engineering & Technology Research Center for Disease-Model Animals, Laboratory Animal Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China.
Conghui ShenGuangdong Engineering & Technology Research Center for Disease-Model Animals, Laboratory Animal Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China.
Honglin RenGuangdong Engineering & Technology Research Center for Disease-Model Animals, Laboratory Animal Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China.
Haiping WangPrenatal Diagnosis Center, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, 510080, Guangdong, China.
Teng WuGuangdong Engineering & Technology Research Center for Disease-Model Animals, Laboratory Animal Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China.
Xinlu FuGuangdong Engineering & Technology Research Center for Disease-Model Animals, Laboratory Animal Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China.
Shijie DengGuangdong Engineering & Technology Research Center for Disease-Model Animals, Laboratory Animal Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China.
Ziqi FengGuangdong Engineering & Technology Research Center for Disease-Model Animals, Laboratory Animal Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China.
Shijie XiongGuangdong Engineering & Technology Research Center for Disease-Model Animals, Laboratory Animal Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China.
Hui LiGuangdong Engineering & Technology Research Center for Disease-Model Animals, Laboratory Animal Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China.
Saifei GaoGuangdong Engineering & Technology Research Center for Disease-Model Animals, Laboratory Animal Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China.
Zhenyu YangGuangdong Engineering & Technology Research Center for Disease-Model Animals, Laboratory Animal Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China.
Fei GaoDurbrain Medical Laboratory, Hangzhou, 310000, Zhejiang, China.
Lele DongDurbrain Medical Laboratory, Hangzhou, 310000, Zhejiang, China.
Jianding ChengDepartment of Forensic Pathology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China.
Weibin CaiGuangdong Engineering & Technology Research Center for Disease-Model Animals, Laboratory Animal Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, Guangdong, China. caiwb@mail.sysu.edu.cn.ORCID 0000-0003-0934-4507
Sun Yat-sen University · CNGuangdong Academy of Medical Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic cardiomyopathy is a primary myocardial injury induced by diabetes with complex pathogenesis. In this study, we identify disordered cardiac retinol metabolism in type 2 diabetic male mice and patients characterized by retinol overload, all-trans retinoic acid deficiency. By supplementing type 2 diabetic male mice with retinol or all-trans retinoic acid, we demonstrate that both cardiac retinol overload and all-trans retinoic acid deficiency promote diabetic cardiomyopathy. Mechanistically, by constructing cardiomyocyte-specific conditional retinol dehydrogenase 10-knockout male mice and overexpressing retinol dehydrogenase 10 in male type 2 diabetic mice via adeno-associated virus, we verify that the reduction in cardiac retinol dehydrogenase 10 is the initiating factor for cardiac retinol metabolism disorder and results in diabetic cardiomyopathy through lipotoxicity and ferroptosis. Therefore, we suggest that the reduction of cardiac retinol dehydrogenase 10 and its mediated disorder of cardiac retinol metabolism is a new mechanism underlying diabetic cardiomyopathy.

Indexed as

Diabetes Mellitus, ExperimentalDiabetes Mellitus, Type 2Diabetic CardiomyopathiesHeart DiseasesMetabolic DiseasesAlcohol OxidoreductasesAnimalsMaleMiceMice, KnockoutMyocytes, CardiacTretinoinVitamin AAlcohol Oxidoreductasesretinol dehydrogenaseTretinoinVitamin A

Identifiers

PMID36864033
PMCPMC9981688
OpenAlexW4322773853

What OpenQuestion 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 OpenQuestion graph.