ArticlePeerJ2026
Post-infarction KLHL40-mediated regulation of cardiac sarcomeric integrity and function.
Article in PeerJ, 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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13 authors.
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Abstract
Background: Cardiac sarcomeric remodeling after myocardial infarction (MI) plays a pivotal role in post-injury cardiac dysfunction, yet the molecular mechanisms governing this process remain incompletely understood. Objective: We aimed to elucidate the role of Kelch-like protein 40 (KLHL40) in sarcomeric protein remodeling and calcium signaling regulation after MI. Methods: By integrating transcriptomic and proteomic datasets with experimental validation, we characterized dynamic changes in KLHL40 expression and its effects on sarcomeric components and myocyte state following hypoxia. KLHL40 expression was evaluated in human post-MI heart tissues and hypoxia-induced H9C2 cells. Functional assays revealed its regulation of key Z-disc-associated proteins (MYOT, CAPZA, and TCAP). Mechanistic candidates were identified Results: KLHL40 expression was markedly upregulated within 6 hours (95% CI [-72.53 to -0.9783]; Conclusion: KLHL40 maintains sarcomeric integrity and cardiomyocyte viability after myocardial infarction by modulating calpain signaling and limiting inflammasome activation and apoptosis. KLHL40 expression and stability are tightly regulated through proteasomal, autophagic, and calpain-dependent pathways.
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