ArticleNature communications2023
Targeting an allosteric site in dynamin-related protein 1 to inhibit Fis1-mediated mitochondrial dysfunction.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 80 citations in OpenAlex.
- The mtROS-Mitophagy Axis: A Decisive Redox Hub Governing Cell Fate in Myocardial Ischemia-Reperfusion Injury.Cardiovascular toxicology · 2026Review
- MST1/Drp1 axis mediates microglia pro-inflammatory activation following cerebral ischemia-reperfusion injury.Scientific reports · 2026Article
- USP33 alleviates FIS1-dependent mitochondrial fission and cardiac microvascular injury in diabetic cardiomyopathy via deubiquitinating and stabilizing ATG7.Cell death & disease · 2026Article
- Dynamin-Related Protein 1 (Drp1) in Inflammatory Bowel Disease: Molecular Pathways Connecting Mitochondrial Dynamics with Intestinal Inflammation and Homeostasis.International journal of molecular sciences · 2026Review
- Pulmonary Vascular Endothelial Cells in Lung Diseases: Mechanisms, Therapeutic Strategies, and Future Directions.Cell proliferation · 2026Review
- Molecular mechanisms of exercise-induced neuroprotection against Parkinson's disease.Sports medicine and health science · 2026Review
- Targeting mitochondria for the treatment of neurodegenerative diseases.Frontiers in neuroscience · 2026Review
- Plant metabolites targeting mitochondrial dysfunction in cardiovascular diseases: pharmacological mechanisms and combination strategies.Frontiers in pharmacology · 2026Review
- Mitochondrial fission and fusion in inflammatory diseases: mechanisms and therapeutic implications.Journal of translational medicine · 2025Review
- Azelastine Inhibits Triple-Negative Breast Cancer Cell Viability via an ARF1-Dependent Mechanism.International journal of molecular sciences · 2025Article
- Small peptide P110 mitigates axonal degeneration of SPG15 patient iPSC-derived neurons by targeting mitochondrial dysfunction.Neurobiology of disease · 2025Article
- Mitochondrial dysfunction in sepsis-induced liver injury: from pathophysiology to preclinical therapeutic targets.Journal of translational medicine · 2025Review
- Inhibition of DRP1-mediated Mitochondrial Fission and NRF2/HO-1/GPX4-mediated Ferroptosis by Mdivi-1 Protects Against Vascular Cognitive Impairment.Molecular neurobiology · 2025Article
- The role of four ERS-related key genes in sepsis induced organ dysfunction and the forewarning model construction.BMC medical informatics and decision making · 2025Article
- The Role of Mitochondrial Dysfunction and Dynamics in Hypertensive Heart Disease: Mechanisms and Recent Advances.Biology · 2025Review
- Pharmacological and Genetic Approaches to Downregulate FIS1 Mitigate Neuropathic Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Excessive mitochondrial fission and associated extracellular mitochondria mediate cardiac dysfunction in obesity cardiomyopathy.Life sciences · 2025Article
- Nutritional Interventions in Amyotrophic Lateral Sclerosis: From Ketogenic Diet and Neuroprotective Nutrients to the Microbiota-Gut-Brain Axis Regulation.Molecular neurobiology · 2025Review
- AIM2 activation mediated by RIPK1/3-dependent mitochondrial DNA release drives AβCell communication and signaling : CCS · 2025Article
- Role of mitochondria in physiological activities, diseases, and therapy.Molecular biomedicine · 2025Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The large cytosolic GTPase, dynamin-related protein 1 (Drp1), mediates both physiological and pathological mitochondrial fission. Cell stress triggers Drp1 binding to mitochondrial Fis1 and subsequently, mitochondrial fragmentation, ROS production, metabolic collapse, and cell death. Because Drp1 also mediates physiological fission by binding to mitochondrial Mff, therapeutics that inhibit pathological fission should spare physiological mitochondrial fission. P110, a peptide inhibitor of Drp1-Fis1 interaction, reduces pathology in numerous models of neurodegeneration, ischemia, and sepsis without blocking the physiological functions of Drp1. Since peptides have pharmacokinetic limitations, we set out to identify small molecules that mimic P110's benefit. We map the P110-binding site to a switch I-adjacent grove (SWAG) on Drp1. Screening for SWAG-binding small molecules identifies SC9, which mimics P110's benefits in cells and a mouse model of endotoxemia. We suggest that the SWAG-binding small molecules discovered in this study may reduce the burden of Drp1-mediated pathologies and potentially pathologies associated with other members of the GTPase family.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.