ArticleGeromedicine2026
Inhibition of PAI-1 shifts cardiomyocyte fate from senescence toward apoptosis and mitigates doxorubicin-induced cardiotoxicity.
Article in Geromedicine, 2026. 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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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.
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Who cites it
1 citing paper in PubMed.
- Postbiotic metabolites fromExperimental and therapeutic medicine · 2026Article
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Authors and funding
9 authors.
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Abstract
Aims: Doxorubicin (Dox) is an effective chemotherapeutic agent, but its clinical use is limited by cardiotoxicity. Cellular senescence contributes to Dox-induced cardiac dysfunction; however, the underlying molecular mechanism mediating the effect of senescence remains poorly understood. This study aimed to identify senescence-associated factors secreted from cardiomyocytes in Dox-treated hearts and define their functional significance in Dox-induced cardiotoxicity. Methods: Mice with cardiomyocyte-specific expression of the endoplasmic reticulum BioID secretome profiling system were used to identify Dox-induced secreted factors. Functional analyses were performed in neonatal rat ventricular myocytes (NRVMs). The effects of plasminogen activator inhibitor-1 (PAI-1) inhibition were evaluated in Dox-treated mice by assessing senescence markers, apoptotic responses, and cardiac structure and function. Results: PAI-1 was identified as a major component of the senescence-associated secretory phenotype and was robustly upregulated in Dox-treated cardiomyocytes. In NRVMs, PAI-1 promoted senescence and maintained the senescent phenotype, in part by conferring resistance to apoptosis. Pharmacological inhibition of PAI-1 reduced senescence markers, enhanced apoptotic responses, and preserved cardiac structure and function in Dox-treated mice. Fate mapping analyses with Conclusion: PAI-1 is a key mediator of Dox-induced cardiac dysfunction. PAI-1 inhibition shifts the fate of cardiomyocytes from senescence toward apoptosis and preserves cardiac structure and function without compromising the antitumor function of Dox, highlighting PAI-1 as a potential therapeutic target for chemotherapy-associated cardiotoxicity.
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