Evidence map›Paper›PMID 39817389›Full record

ArticleCurrent cancer drug targets2025

Value of Label-Free Ubiquitin-Proteomic Analysis on Defining the Protective Mechanism of Valsartan against Doxorubicin-Induced Heart Failure.

Liyuan Zhang, Yujing Zhang, Di Chen, Shujuan Shao, Qin Yu

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Article in Current cancer drug targets, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

What it found

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3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Liyuan ZhangDepartment of Cardiology, Affiliated Zhongshan Hospital of Dalian University, Dalian 116001, Liaoning, China.
Yujing ZhangKey Laboratory for Proteomics of Liaoning Province, Dalian Medical University, Lvshun South Road No. 9, Dalian 116044, Liaoning, China.
Di ChenDepartment of Cardiology, Affiliated Zhongshan Hospital of Dalian University, Dalian 116001, Liaoning, China.
Shujuan ShaoKey Laboratory for Proteomics of Liaoning Province, Dalian Medical University, Lvshun South Road No. 9, Dalian 116044, Liaoning, China.
Qin YuDepartment of Cardiology, Affiliated Zhongshan Hospital of Dalian University, Dalian 116001, Liaoning, China.

Funding

Liaoning Revitalization Talents Program XLYC2007122National Natural Science Foundation of China 21974017
6 · The paper itself

Abstract

introductionThe cardiotoxicity and subsequent Heart Failure (HF) induced by Doxorubicin (DOX) limit the clinical application of DOX. Valsartan (Val) is an angiotensin II receptor blocker that could attenuate the HF induced by DOX. However, the underlying mechanism of Val in this process is not fully understood.

methodsIn this study, we explored the cardio-protective mechanism of Val against DOX-induced cardiotoxicity using label-free ubiquitin-proteomic analysis.

resultsResults showed that 27 lysine-ubiquitination sites in 25 proteins were differentially expressed between DOX and DOX+Val treated groups. In addition, the levels of ubiquitin modification of the myosin family and Ankrd1 were upregulated post-Val. Val also in-creased ATP production and activated the Akt/mTOR pathway by regulating the sarcoplas-mic/endoplasmic reticulum calcium ATPase (SERCA2a) and cardiomyocyte calcium hemo-stasis.

conclusionThe results highlight the value of label-free ubiquitin-proteomic analysis in defining the molecular mechanism of Val against HF and may be helpful in the development of new therapeutic agents for HF via targeting molecules defined in this research.

Indexed as

Cardiotonic AgentsCardiotoxicityDoxorubicinHeart FailureValsartanAnimalsMaleProteomicsRatsRats, Sprague-DawleyUbiquitinUbiquitinationCardiotonic AgentsDoxorubicinUbiquitinValsartanAkt/mTOR pathway.cardiotoxicityDoxorubicinheart failureubiquitin-proteomicsvalsartan

Identifiers

PMID39817389

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