Enhanced Drp1 activity mediates excessive mitochondrial fission, contributing to the onset and progression of various chronic diseases, including neurodegenerative, cardiovascular, and metabolic disorders. Studies indicate that exercise mitigates mitochondrial dysfunction by modulating Drp1-related signaling targets, thereby inhibiting Drp1 activity and reducing excessive mitochondrial fission. This, in turn, enhances mitochondrial function and cellular metabolism. This review synthesizes the current understanding of Drp1 structure and activation mechanisms, and analyzes the effects of exercise interventions on Drp1-mediated mitochondrial fission in different disease models to improve common chronic conditions. This research deepens our insight into the specific mechanisms of Drp1-induced excessive mitochondrial fission in chronic disease pathogenesis, offering new theoretical support and practical guidance for exercise as a non-pharmacological intervention strategy.
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http://dx.doi.org/10.3389/fcell.2025.1481756 | DOI Listing |
Front Cell Dev Biol
February 2025
School of Exercise and Health Sciences, Tianjin University of Sport, Tianjin, China.
Enhanced Drp1 activity mediates excessive mitochondrial fission, contributing to the onset and progression of various chronic diseases, including neurodegenerative, cardiovascular, and metabolic disorders. Studies indicate that exercise mitigates mitochondrial dysfunction by modulating Drp1-related signaling targets, thereby inhibiting Drp1 activity and reducing excessive mitochondrial fission. This, in turn, enhances mitochondrial function and cellular metabolism.
View Article and Find Full Text PDFFront Pharmacol
February 2025
Department of Core Facility, The First Hospital of Jilin University, Changchun, Jilin, China.
Drug resistance is a prevalent challenge in clinical disease treatment, often leading to disease relapse and poor prognosis. Therefore, it is crucial to gain a deeper understanding of the molecular mechanisms underlying drug resistance and to develop targeted strategies for its effective prevention and management. Mitochondria, as vital energy-producing organelles within cells, have been recognized as key regulators of drug sensitivity.
View Article and Find Full Text PDFInt J Mol Sci
March 2025
Department of Medicine, Surgery and Dentistry, University of Salerno "Scuola Medica Salernitana", 84081 Baronissi, Italy.
G protein-coupled receptors (GPCRs) represent a family of membrane proteins that regulate several cellular processes. Among the GPCRs, G protein-coupled receptor kinases (GRKs) regulate downstream signaling pathways and receptor desensitization. GRK2 has gained significant interest due to its cardiovascular physiology and pathological involvement.
View Article and Find Full Text PDFInt J Mol Sci
February 2025
Department of Medical Biology, Faculty of Medicine, Medical University-Plovdiv, 4000 Plovdiv, Bulgaria.
Autism spectrum disorder (ASD) is a group of neurodevelopmental and biobehavioral conditions that arises from complex interactions between environmental factors and physiological development in genetically predisposed individuals. Among the most frequently observed metabolic abnormalities in ASD is mitochondrial dysfunction. Mitochondria respond to cellular stress by altering their dynamics or initiating mitophagy.
View Article and Find Full Text PDFInt J Mol Sci
February 2025
Department of Molecular Biology, Princeton University, Princeton, NJ 08544, USA.
Mitochondria are involved in a wide array of critical cellular processes from energy production to cell death. The morphology (size and shape) of mitochondrial compartments is highly responsive to both intracellular and extracellular conditions, making these organelles highly dynamic. Nutrient levels and stressors both inside and outside the cell inform the balance of mitochondrial fission and fusion and the recycling of mitochondrial components known as mitophagy.
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