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Review
. 2025 Jun 4:13:1615363.
doi: 10.3389/fpubh.2025.1615363. eCollection 2025.

Effects of atmospherically relevant PM2.5 on skeletal muscle mitochondria: a review of damage mechanisms and potential of exercise interventions

Yi Ding #  1 , Qiliang Wan #  1 , Wenduo Liu  1
Affiliations
Review

Effects of atmospherically relevant PM2.5 on skeletal muscle mitochondria: a review of damage mechanisms and potential of exercise interventions

Yi Ding et al. Front Public Health. .

Abstract

This study aims to explore the multifaceted impacts and mechanisms of fine particulate matter (PM2.5) exposure on skeletal muscle mitochondria. Evidence suggests that PM2.5 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, PM2.5 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 PM2.5 exposure and the preventive and treatment potential of exercise.

Keywords: exercise; fine dust; mitochondrial function; particulate matter; skeletal muscle.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Schematic representation of skeletal muscle mitochondrial morphological damage induced by PM2.5 exposure. Including alterations in cristae structure, outer/inner membrane integrity, and increased mitochondrial fission activity. Created using Figdraw (ID: USTTAec5f8).
Figure 2
Figure 2
Schematic representation of skeletal muscle mitochondrial dysfunction induced by PM2.5 exposure. Including disrupted mitochondrial biogenesis signaling, increased ROS production, and reduced electron transport efficiency, leading to decreased mitochondrial respiration rate, membrane potential, and ATP synthesis. Created using Figdraw (ID: WSTWS9999d).
Figure 3
Figure 3
Schematic representation of the protective role of endurance exercise against skeletal muscle mitochondrial dysfunction induced by PM2.5 exposure. Exercise promotes mitochondrial biogenesis, mitophagy, and antioxidant defense, enhancing mitochondrial homeostasis and counteracting PM2.5-induced oxidative stress and damage. Created using Figdraw (ID: PWSAW4e4ee).
See this image and copyright information in PMC

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