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February 12, 2026Redox Report0 citationsOpen Access

Endogenous H₂S promotes HSPA8 sulfhydration to downregulate HIF1α and prevent ferroptosis in septic myocardial injury

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DJDu JiankuiSZSheng ZhangLZLi Zhang

Key Points

  • This research aims to explore the role of endogenous H₂S in preventing ferroptosis and myocardial injury during sepsis.
  • Characterized the H₂S-HSPA8-HIF1α-BNIP3 pathway in myocardial injury
  • Investigated protein sulfhydration as a cardioprotective mechanism
  • Assessed the therapeutic potential of Allicin in septic cardiomyopathy.
  • Established a novel axis involving H₂S, HSPA8, and HIF1α
  • Demonstrated that sulfhydration helps downregulate HIF1α
  • Showed Allicin's potential as a treatment for septic myocardial injury.

Abstract

This 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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Cite This Study

Jiankui et al. (2026) studied this question.

synapsesocial.com/papers/698d6e5a5be6419ac0d5407fhttps://doi.org/10.1080/13510002.2026.2626159
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