Key result
PM2.5 exposure impairs skeletal muscle mitochondria, while endurance exercise helps mitigate this damage.
Why the study?
This study aims to explore the multifaceted impacts and mechanisms of fine particulate matter (PM 2.5) exposure on skeletal muscle mitochondria.
PM2.5 exposure impairs skeletal muscle mitochondrial morphology and function, disrupting glucose and lipid metabolism.
Supports potential exercise mitigation of PM2.5 mitochondrial effects; leaves open prospective human trials.
This study aims to explore the multifaceted impacts and mechanisms of fine particulate matter (PM 2.5 ) exposure on skeletal muscle mitochondria. Evidence suggests that PM 2.5 can penetrate the respiratory barrier and enter the circulatory system, spreading throughout the body and causing significant damage to the morphology, quantity, and function of skeletal muscle mitochondria. This is manifested by a decline in oxidative phosphorylation efficiency and mitochondrial dysfunction. Meanwhile, PM 2.5 exposure induces excessive production of reactive oxygen species, triggering oxidative stress responses that impair mitochondrial dynamic regulation. This further disrupts the balance of glucose and lipid metabolism in skeletal muscle, exacerbating the development of metabolic diseases. The review underscores the systemic effects on skeletal muscle following mitochondrial dysfunction after PM 2.5 exposure and the preventive and treatment potential of exercise.
No takes yet. Share an insight, caveat, or question.
Ding et al. (2025) conducted a review in PM2.5 exposure-induced skeletal muscle mitochondrial damage. Exercise interventions was evaluated. PM2.5 exposure impairs skeletal muscle mitochondrial morphology and function, while endurance exercise interventions demonstrate potential in preventing and mitigating this damage.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: