ArticleNature communications2025
Polysulfur-based bulking of dynamin-related protein 1 prevents ischemic sulfide catabolism and heart failure in mice.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Multiscale interactions in cardiovascular homeostasis and remodeling: from molecular coupling to organelle and multicellular networks.The journal of physiological sciences : JPS · 2026Review
- Hydrogen Sulphide Signalling in Plants: From Persulfidation to Metabolic Regulation and Stress Response.Plant, cell & environment · 2026Review
- Sheep-derived probiotics alleviate weaning-induced oxidative stress in lambs via the gut-liver axis.NPJ biofilms and microbiomes · 2026Article
- Ultrasensitive bioorthogonal probes for selective discrimination of trace HActa pharmaceutica Sinica. B · 2026Article
- Formation of a reducing microenvironment and regulation of protein supersulfidation by gut microbial supersulfides.Redox biology · 2026Article
- Sulfide:quinone oxidoreductase drives mitochondrial supersulfide metabolism to regulate bioenergetics and longevity in eukaryotes.bioRxiv : the preprint server for biology · 2026Article
- Trimetallic Nanozyme-Embedded Smart Hydrogel Enables NIR-Controlled Bacterial Killing and Oxidative Stress Alleviation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Supersulfide donors and their therapeutic targets in inflammatory diseases.Frontiers in immunology · 2025Review
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Authors and funding
16 authors.
Funding
Abstract
The presence of redox-active molecules containing catenated sulfur atoms (supersulfides) in living organisms has led to a review of the concepts of redox biology and its translational strategy. Glutathione (GSH) is the body's primary detoxifier and antioxidant, and its oxidized form (GSSG) has been considered as a marker of oxidative status. However, we report that GSSG, but not reduced GSH, prevents ischemic supersulfide catabolism-associated heart failure in male mice by electrophilic modification of dynamin-related protein (Drp1). In healthy exercised hearts, the redox-sensitive Cys644 of Drp1 is highly S-glutathionylated. Nearly 40% of Cys644 is normally polysulfidated, which is a preferential target for GSSG-mediated S-glutathionylation. Cys644 S-glutathionylation is resistant to Drp1 depolysulfidation-dependent mitochondrial hyperfission and myocardial dysfunction caused by hypoxic stress. MD simulation of Drp1 structure and site-directed mutagenetic analysis reveal a functional interaction between Cys644 and a critical phosphorylation site Ser637, through Glu640. Bulky modification at Cys644 via polysulfidation or S-glutathionylation reduces Drp1 activity by disrupting Ser637-Glu640-Cys644 interaction. Disruption of Cys644 S-glutathionylation nullifies the cardioprotective effect of GSSG against heart failure after myocardial infarction. Our findings suggest a therapeutic potential of supersulfide-based Cys bulking on Drp1 for ischemic heart disease.
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