ArticleNature communications2025
A hidden cysteine in Fis1 targeted to prevent excessive mitochondrial fission and dysfunction under oxidative stress.
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 9 papers.
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Who cites it
9 citing papers in PubMed.
- Cytosolic PRDX1 acts as an extramitochondrial sink to set mitochondrial HRedox biology · 2026Article
- Multidimensional Unraveling Insights from an Enzyme-Nanozyme Cascade-Based Electrochemical Biosensor for Screening Microplastic Neurotoxicity.Environment & health (Washington, D.C.) · 2026Article
- ALCAT1 promotes diabetic cardiomyopathy by linking myocardial tetralinoleoyl cardiolipin deficiency to lipotoxicity.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Gram-negative bacterial outer membrane proteins and lipopolysaccharides key factors linking chicken coop environment and oxidative stress.Redox biology · 2026Review
- Integrating multi-omics and network toxicology to identify FIS1 as a key target of environmental pollutants in male infertility.Frontiers in cell and developmental biology · 2026Article
- FIS1 dependent peripheral fission exacerbates mitochondrial fragmentation and dysfunction in prion diseases.Frontiers in neuroscience · 2026Article
- Subcellular Stress Markers in Epithelial Ovarian Cancer.International journal of molecular sciences · 2025Review
- A role for Fis1 in dendritic development.Scientific reports · 2025Article
- Mesenchymal stem cells inhibit mitochondrial fission by upregulating armadillo repeat containing 1, ameliorating oxidative stress in renal fibrosis.Stem cell research & therapy · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fis1-mediated mitochondrial localization of Drp1 and excessive mitochondrial fission occur in human pathologies associated with oxidative stress. However, it is not known how Fis1 detects oxidative stress and what structural changes in Fis1 enable mitochondrial recruitment of Drp1. We find that conformational change involving α1 helix in Fis1 exposes its only cysteine, Cys41. In the presence of oxidative stress, the exposed Cys41 in activated Fis1 forms a disulfide bridge and the Fis1 covalent homodimers cause increased mitochondrial fission through increased Drp1 recruitment to mitochondria. Our discovery of a small molecule, SP11, that binds only to activated Fis1 by engaging Cys41, and data from genetically engineered cell lines lacking Cys41 strongly suggest a role of Fis1 homodimerization in Drp1 recruitment to mitochondria and excessive mitochondrial fission. The structure of activated Fis1-SP11 complex further confirms these insights related to Cys41 being the sensor for oxidative stress. Importantly, SP11 preserves mitochondrial integrity and function in cells during oxidative stress and thus may serve as a candidate molecule for the development of treatment for diseases with underlying Fis1-mediated mitochondrial fragmentation and dysfunction.
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