ArticleHereditas2025
USP8 protects rat-derived H9C2 cardiomyocytes from doxorubicin-triggered ferroptosis and cell death through deubiquitination-mediated stabilization of MDM4.
Article in Hereditas, 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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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.
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3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute heart failure (AHF) is a life-threatening clinical syndrome due to impaired cardiac function. Ferroptosis has emerged as a contributor to cytotoxicity in cardiomyocytes. However, the functional interplay between USP8 and ferroptosis during AHF has not been investigated.
methodsH9C2 rat cardiomyocytes were treated with doxorubicin (Dox) to establish an experimental model. Cell cytotoxicity was evaluated by measuring cell viability, LDH release, and cell death. Ferroptosis was assessed by analyzing Fe
resultsUSP8 and MDM4 were downregulated in Dox-exposed H9C2 cardiomyocytes. USP8 overexpression alleviated Dox-triggered cytotoxicity and cell death in H9C2 cardiomyocytes. Moreover, USP8 overexpression mitigated H9C2 cardiomyocyte ferroptosis induced by Dox. Mechanistically, USP8 stabilized MDM4 via deubiquitination. Inhibition of MDM4 counteracted the ability of USP8 overexpression to attenuate Dox-triggered cell death and ferroptosis in H9C2 cardiomyocytes.
conclusionOur findings indicate that USP8 overexpression protects H9C2 cardiomyocytes from Dox-induced ferroptosis by stabilizing MDM4 via deubiquitination.
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