ArticleFrontiers in pharmacology2026
PMEPA1 attenuates myocardial ischemia-reperfusion injury via interaction with NEDD4 and involvement of the TGF-β/SMAD pathway.
Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Myocardial ischemia-reperfusion injury (MIRI) remains a significant challenge in cardiovascular medicine, and its molecular mechanisms are not yet fully elucidated. Methods: In the present study, integrated transcriptomic analysis combined with machine learning identified PMEPA1 as a key gene consistently downregulated in both rat models of MIRI and H9c2 cardiomyocytes subjected to ischemia -reperfusion injury. A series of Results: Overexpression of PMEPA1 enhanced cardiomyocyte proliferation, reduced apoptosis, and inhibited activation of the TGF-β/SMAD signaling pathway. Further investigation revealed a direct interaction between PMEPA1 and the E3 ubiquitin ligase NEDD4. Both NEDD4 overexpression and PMEPA1 knockdown aggravated cardiomyocyte injury and increased activation of the TGF-β/SMAD pathway. Notably, the detrimental effects of NEDD4 overexpression were attenuated in the absence of PMEPA1, suggesting a PMEPA1-dependent mechanism. Discussion: These findings highlight a novel NEDD4-PMEPA1 axis in the regulation of TGF-β/SMAD signaling during myocardial injury and provide new insights into potential molecular targets for the treatment of cardiovascular disease.
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