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Epigenetic erosion of H4K20me1 induced by inflammation drives aged stem cell ferroptosis

Roméo S Blanc1,2, Nidhi Shah3, Sarah Hachmer4

  • 1Department of Cell and Regenerative Biology, University of Wisconsin-Madison, Madison, WI, USA. rblanc@wisc.edu.

Nature Aging
|June 30, 2025
PubMed

Insights

Systemic inflammation accelerates aging in muscle stem cells (MuSCs) by causing epigenetic changes that lead to ferroptosis. Inhibiting inflammation preserves MuSC function and improves muscle health in aging.

Area of Science:

  • Gerontology
  • Epigenetics
  • Stem Cell Biology

Background:

  • Aging leads to reduced stem cell function and numbers.
  • Systemic inflammation is a hallmark of aging and impacts tissue regeneration.

Purpose of the Study:

  • To investigate the mechanism linking systemic inflammation to muscle stem cell (MuSC) aging.
  • To identify epigenetic alterations driving MuSC dysfunction and ferroptosis in aging.

Main Methods:

  • Analysis of H4K20 monomethylation levels in MuSCs from aged and young mice.
  • Investigation of Kmt5a expression and its role in regulating H4K20me1.
  • Assessment of ferroptosis markers, iron metabolism, and reactive oxygen species in MuSCs.
  • Intervention study involving long-term inhibition of systemic inflammation in aged mice.

Main Results:

  • Age-related inflammation decreases H4K20 monomethylation in MuSCs.
  • Inflammatory signals downregulate Kmt5a, leading to epigenetic silencing of anti-ferroptosis genes.
  • Aged MuSCs exhibit ferroptosis, aberrant iron metabolism, increased ROS, and lipid peroxidation.
  • Inhibition of inflammation prevents ferroptosis, preserves MuSC numbers, and enhances muscle regeneration.

Conclusions:

  • Epigenetic erosion, specifically reduced H4K20me1, links inflammation to MuSC aging and ferroptosis.
  • Targeting inflammation offers a therapeutic strategy to counteract age-related muscle degeneration.

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