Evidence map›Paper›PMID 41496210›Full record

ArticleRedox biology2026

USP13 ameliorates myocardial infarction injury by inhibiting ferroptosis via stabilizing ALDOA.

Pengcheng Li, Delong Chen, Chenyun Zhang, Qinyan Gong, Abuduwufuer Yidilisi, Jiacheng Fang, Yuxuan Zhang, Junyan Jin, Jiniu Huang, Jun Jiang

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Redox biology, 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

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

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

10 authors.

Pengcheng LiDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China; State Key Laboratory of Transvascular Implantation Devices, Hangzhou, 310009, China; Heart Regeneration and Repair Key Laboratory of Zhejiang Province, Hangzhou, 310009, China.
Delong ChenDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China; State Key Laboratory of Transvascular Implantation Devices, Hangzhou, 310009, China; Heart Regeneration and Repair Key Laboratory of Zhejiang Province, Hangzhou, 310009, China.
Chenyun ZhangDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China; State Key Laboratory of Transvascular Implantation Devices, Hangzhou, 310009, China; Heart Regeneration and Repair Key Laboratory of Zhejiang Province, Hangzhou, 310009, China.
Qinyan GongDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China; State Key Laboratory of Transvascular Implantation Devices, Hangzhou, 310009, China; Heart Regeneration and Repair Key Laboratory of Zhejiang Province, Hangzhou, 310009, China.
Abuduwufuer YidilisiDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China; State Key Laboratory of Transvascular Implantation Devices, Hangzhou, 310009, China; Heart Regeneration and Repair Key Laboratory of Zhejiang Province, Hangzhou, 310009, China.
Jiacheng FangDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China; State Key Laboratory of Transvascular Implantation Devices, Hangzhou, 310009, China; Heart Regeneration and Repair Key Laboratory of Zhejiang Province, Hangzhou, 310009, China.
Yuxuan ZhangDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China; State Key Laboratory of Transvascular Implantation Devices, Hangzhou, 310009, China; Heart Regeneration and Repair Key Laboratory of Zhejiang Province, Hangzhou, 310009, China.
Junyan JinDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China; State Key Laboratory of Transvascular Implantation Devices, Hangzhou, 310009, China; Heart Regeneration and Repair Key Laboratory of Zhejiang Province, Hangzhou, 310009, China.
Jiniu HuangDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China; State Key Laboratory of Transvascular Implantation Devices, Hangzhou, 310009, China; Heart Regeneration and Repair Key Laboratory of Zhejiang Province, Hangzhou, 310009, China. Electronic address: 12118191@zju.edu.cn.
Jun JiangDepartment of Cardiology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, 310009, China; State Key Laboratory of Transvascular Implantation Devices, Hangzhou, 310009, China; Heart Regeneration and Repair Key Laboratory of Zhejiang Province, Hangzhou, 310009, China; Transvascular Implantation Devices Research Institute, Hangzhou, 310053, China. Electronic address: jiang-jun@zju.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite the central role of deubiquitinases (DUBs) in maintaining protein homeostasis, their important role in post-myocardial infarction (MI) remodeling remains incompletely characterized. Our study identifies a DUB, ubiquitin-specific protease 13 (USP13), as a stress-responsive regulator exhibiting significant downregulation in MI-induced cardiac injury. USP13 deficiency aggravated cardiac ferroptosis and cardiac dysfunction after MI surgery. Mechanistically, USP13 directly bound to fructose-bisphosphate aldolase A (ALDOA) via its ubiquitin-specific protease domain. USP13 regulated K48-linked deubiquitination and the stability of ALDOA at K13, thereby preventing its degradation via the proteasomal pathway and restraining ferroptosis in cardiomyocytes. Moreover, specifical overexpression the endogenous USP13 in mouse hearts attenuated MI-induced cardiac injury. We confirmed that USP13 inhibited MI-induced cardiac injury by deubiquitinating and stabilizing ALDOA. These findings suggest that USP13 may serve as a promising therapeutic target for myocardial infarction, providing a foundation for developing novel treatment strategies focused on ferroptosis.

Indexed as

FerroptosisFructose-Bisphosphate AldolaseMyocardial InfarctionUbiquitin-Specific ProteasesAnimalsDisease Models, AnimalHumansMaleMiceMyocytes, CardiacUbiquitinationFructose-Bisphosphate AldolaseUbiquitin-Specific ProteasesUSP13 protein, humanCardiac injuryMyocardial infarctUbiquitinationUSP13

Identifiers

PMID41496210
PMCPMC12808845

What OpenQuestion holds

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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.