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Atmospherically relevant PM2.5 promotes age-related muscle atrophy in an age-dependent manner

  • Zilin Wang
  • , Wenduo Liu
  • , Sang Hyun Kim*
  • *Corresponding author for this work
  • Beihua University
  • Jeonbuk National University

Research output: Contribution to journalJournal articlepeer-review

Abstract

Background: Maintaining the quality and function of skeletal muscle in the older adult has become a key topic in successful aging. However, the impact of environmental factors on skeletal muscle aging is often overlooked. Methods: This study used male mice aged 1, 6, and 15 months, which were each exposed to PM2.5 (50 μg/m3, 2 h/day) for 5 days, and the skeletal muscles of each age group were analyzed one month after the end of the treatment to verify the age-specific effects of PM2.5 on the skeletal muscle system. Results: Total body weight and lean body weight were significantly affected by age and PM2.5 exposure. However, fat levels were not affected by PM2.5 exposure. PM2.5 exposure promoted the development of age-related muscle atrophy by inducing oxidative stress and increased expression of Myostatin in skeletal muscle of older adults. On the other hand, the damaging effect of PM2.5 exposure on skeletal muscle mitochondria was age-related. Young and older adult mice showed extensive mitochondrial damage after PM2.5 exposure. In particular, older adults showed a marked increase in mitochondrial fission and mitophagy after PM2.5 exposure. Conclusions: The effects of PM2.5 exposure on the skeletal muscle system are age-specific, with distinct damaging effects during growth and aging, whereas skeletal muscles in middle-aged mice are resistant to PM2.5-induced damage.

Original languageEnglish
Article number113091
JournalExperimental Gerontology
Volume217
DOIs
StatePublished - 2026.05

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

Keywords

  • Age groups
  • Air pollution
  • Atrophy
  • Mitochondrial damage
  • Mitophagy

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