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Aging Impairs Macrophage Phagocytosis Through Mitochondrial ROS-Induced Collagen Production

Yuming Wang1,2, Xin Xu3,4, Nuanqin Shen3,4

  • 1Department of Geriatrics, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.

Aging Cell
|June 16, 2026
PubMed

Insights

Aging impairs macrophage phagocytosis by increasing collagen production, driven by mitochondrial ROS. MitoTEMPO treatment rejuvenates this immune function by restoring actin dynamics and boosting bacterial clearance in aged mice.

Area of Science:

  • Immunology
  • Cell Biology
  • Aging Research

Background:

  • Macrophages are crucial immune cells with phagocytic functions.
  • The effects of aging on macrophage phagocytosis are not well understood.
  • Phagocytosis is essential for immune defense and tissue homeostasis.

Purpose of the Study:

  • To investigate the impact of aging on macrophage phagocytic activity.
  • To elucidate the molecular mechanisms underlying age-related decline in phagocytosis.
  • To identify potential therapeutic targets for enhancing immune function in aging.

Main Methods:

  • In vitro and in vivo phagocytic assays using human and mouse macrophages.
  • RNA-sequencing (RNA-seq) to analyze gene expression changes in aged macrophages.
  • Protein interaction assays to study collagen-actin binding.
  • Mitochondrial reactive oxygen species (ROS) measurement and manipulation.
  • In vivo mouse models to assess therapeutic interventions.

Main Results:

  • Aged macrophages exhibited significantly reduced phagocytic activity compared to young macrophages.
  • Upregulated expression of extracellular matrix genes, particularly collagens (e.g., COL1A1), was observed in aged macrophages.
  • Collagen was found to bind to actin filaments, inhibiting F-actin turnover and impairing phagocytosis.
  • Mitochondrial ROS drives collagen overproduction in aged macrophages.
  • MitoTEMPO treatment rejuvenated macrophage phagocytosis by restoring actin dynamics and enhancing bacterial clearance in vivo.

Conclusions:

  • Aging impairs macrophage phagocytosis through collagen accumulation and disrupted actin dynamics.
  • Mitochondrial ROS plays a key role in driving collagen overproduction and phagocytic dysfunction.
  • MitoTEMPO shows potential as a therapeutic agent to restore macrophage function and promote healthy immune aging.

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