What this means
Scientists lowered a fat called cardiolipin in young mice and saw aging-like muscle changes. Restoring it in adult mice reversed some muscle loss and prevented early death.
Plain-English summary written by an AI model from the abstract. The original is below.
- Who it was tested in
- Mice and human muscle samples
- Kind of research
- A study
The science
- Original title
- Mitochondrial membrane lipid cardiolipin controls fiber-type adaptations in aging muscle via estrogen-related receptor γ.
- Authors
- Finger F, Frost M, Watanabe S et al.
- Journal
- Nature aging
- Published
- Sep 29, 2026
- Study type
- Study · in humans
- PMID
- 42811121 ↗
Abstract
Aging paradoxically leads to both a decline in skeletal muscle mitochondrial function and a shift in muscle composition that favors fibers rich in mitochondria. Yet the biological rationale and mechanism underlying this phenomenon remain largely unknown. Here we show that synthesis of the mitochondrial membrane lipid, cardiolipin, causally links mitochondrial dysfunction to fiber-type adaptations in aging mouse and human skeletal muscle. By mimicking the aging decline of skeletal muscle cardiolipin levels in young mice using inducible tissue-specific cardiolipin synthase 1 (Crls1) deletion, we could reproduce key aging hallmarks, including the shift from glycolytic to oxidative fibers. This shift is mediated by mitochondria-to-nucleus signaling through the nuclear receptor, estrogen-related receptor γ, which promotes reactive oxygen species-sensitive glucose uptake and enhanced glycolytic rerouting to sustain antioxidant defenses. Restoring Crls1 expression in adult Crls1 knockout mice reestablishes cardiolipin levels, initiates reversal of muscle atrophy and fully rescues premature mortality. These findings reveal how changes in a mitochondrial membrane lipid cell autonomously orchestrate fiber-type adaptations in aging and myopathies.
Finger F, Frost M, Watanabe S et al. Mitochondrial membrane lipid cardiolipin controls fiber-type adaptations in aging muscle via estrogen-related receptor γ. Nature aging. 2026. doi:10.1038/s43587-026-01227-7. PMID: 42811121. https://pubmed.ncbi.nlm.nih.gov/42811121/
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