ArticleRedox report : communications in free radical research2026
Endogenous H₂S promotes HSPA8 sulfhydration to downregulate HIF1α and prevent ferroptosis in septic myocardial injury.
Article in Redox report : communications in free radical research, 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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8 authors.
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Abstract
backgroundSepsis-induced myocardial injury (SIMI) contributes significantly to morbidity and mortality in sepsis, but its molecular mechanisms are not fully understood. Hydrogen sulfide (H₂S), an endogenous signaling molecule, regulates inflammation, oxidative stress, and cell death in cardiovascular diseases, with protein sulfhydration as a key mechanism.
methodsWe used in vitro and in vivo sepsis models we investigated the protective to examine the effects of H₂S donors (GYY4137 and Allicin) on SIMI. We focused on ferroptosis and the HIF1α/BNIP3 axis, and applied transcriptomic, proteomic, and molecular biology approaches.
resultsSepsis suppressed the CSE/H₂S pathway, increasing ferroptosis and myocardial injury. Exogenous H₂S attenuated cardiac dysfunction, inflammation, and cell death. Mechanistically, H₂S promoted HSPA8 sulfhydration at Cys574, enhancing HIF1α degradation and inhibiting BNIP3, thereby reducing oxidative stress, ferroptosis, and myocardial damage. Allicin, a natural H₂S donor, induced endogenous H₂S production, restored HSPA8 sulfhydration, and provided cardioprotection without toxicity.
conclusionThis study reveals a novel H₂S-HSPA8-HIF1α-BNIP3 axis in regulating ferroptosis and myocardial injury during sepsis. Protein sulfhydration mediates the cardioprotective effects of H₂S, and Allicin emerges as a promising therapeutic agent for septic cardiomyopathy.
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