Evidence map›Paper›PMID 41794713›Full record

ArticleCardiovascular diabetology2026

Dusp15 modulates mtHsp70 Thr116 phosphorylation state to preserve mito-UPR and attenuate cardiac dysfunction in diabetic cardiomyopathy.

Yan Liu, Hongshuo Shi, Chun Li, Haowen Zhuang, Yinglong Li, Xiuling He, Ying Jiang, Zhiyu Jin, Zhijiang Guo, Sangbing Ong and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cardiovascular diabetology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

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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

1 citing paper in PubMed.

  1. 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

14 authors.

Yan Liu *State Key Laboratory for Innovation and Transformation of Luobing Theory, Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province, Department of Cardiology, Qilu Hospital of Shandong University, Jinan, 250012, China.
Hongshuo Shi *Shandong University of Traditional Chinese Medicine, Jinan, China.
Chun Li *School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, China.
Haowen ZhuangSchool of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, China.
Yinglong LiSchool of Public Health, Dali University, Dali, 671000, Yunnan, China.
Xiuling HeDepartment of Cardiology, School of Medicine, South China University of Technology, Guangzhou, 510006, China.
Ying JiangDepartment of Cardiology, School of Medicine, South China University of Technology, Guangzhou, 510006, China.
Zhiyu JinDepartment of Cardiology, School of Medicine, South China University of Technology, Guangzhou, 510006, China.
Zhijiang GuoThe Chinese University of Hong Kong, Shatin, Hong Kong, SAR, China.
Sangbing OngThe Chinese University of Hong Kong, Shatin, Hong Kong, SAR, China.
Yuanyuan WangState Key Laboratory for Innovation and Transformation of Luobing Theory, Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province, Department of Cardiology, Qilu Hospital of Shandong University, Jinan, 250012, China.
Xing ChangGuang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, 100053, China. xingchang_tcm@outlook.com.
Guipeng AnState Key Laboratory for Innovation and Transformation of Luobing Theory, Key Laboratory of Cardiovascular Remodeling and Function Research of MOE, NHC, CAMS and Shandong Province, Department of Cardiology, Qilu Hospital of Shandong University, Jinan, 250012, China. guipengan@hotmail.com.
Junyan WangSchool of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, 510006, Guangdong, China. wangjunyan@gzucm.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetic cardiomyopathy (DCM) involves cardiac dysfunction/remodeling with mitochondrial stress and impaired mitochondrial proteostasis. The role of dual-specificity phosphatases (DUSPs) in these processes remains unclear. We examined whether Dusp15 modulates diabetic cardiac injury and whether mtHsp70/mito-UPR-linked proteostasis is involved.

methodsDCM was induced in mice by high-fat diet (HFD) combined with low-dose streptozotocin (STZ). We studied cardiomyocyte-specific Dusp15 knockout (Dusp15

resultsDusp15 was reduced in diabetic hearts and associated with impaired contractility. Dusp15 gain-of-function improved cardiac function and reduced remodeling/inflammation, whereas Dusp15

conclusionDusp15 is a stress-responsive regulator that protects against diabetic cardiac dysfunction and remodeling through mtHsp70-associated mito-UPR signaling. Targeting the Dusp15-mtHsp70 axis may represent a therapeutic strategy for diabetic cardiomyopathy.

Indexed as

Diabetes Mellitus, ExperimentalDiabetic CardiomyopathiesDual-Specificity PhosphatasesHSP70 Heat-Shock ProteinsMitochondria, HeartMitochondrial ProteinsMyocytes, CardiacUnfolded Protein ResponseVentricular Function, LeftAnimalsCell LineMaleMice, Inbred C57BLMice, KnockoutMyocardial ContractionPhosphorylationDual-Specificity PhosphatasesHSP70 Heat-Shock ProteinsMitochondrial ProteinsDiabetic cardiomyopathyDusp15Mitochondrial unfolded protein responsemtHsp70

Identifiers

PMID41794713
PMCPMC13020309

What Socratic holds

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LicenceCC BY-NC-ND
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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 Socratic graph.