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Updated: Apr 10, 2026

Author Spotlight: Unveiling Mitochondrial Function and Cellular Metabolic Adaptation in Metabolic Diseases
Published on: October 4, 2024
Oxidative proteome alterations during skeletal muscle ageing.
Sofia Lourenço Dos Santos1, Martin A Baraibar1, Staffan Lundberg2
1Sorbonne Universités, UPMC Univ Paris 06, UMR 8256, Biological Adaptation and Ageing-IBPS, Paris F-75005, France; CNRS UMR-8256, Paris F-75005, France; Inserm U1164, Paris F-75005, France.
Oxidative stress damages proteins in aging skeletal muscle, contributing to sarcopenia. Identifying these oxidized proteins offers insights into muscle aging mechanisms and potential therapeutic targets.
Area of Science:
- Gerontology
- Molecular Biology
- Muscle Physiology
Background:
- Sarcopenia, the age-related loss of muscle mass and strength, significantly impairs mobility and quality of life.
- Cellular aging is characterized by accumulating oxidatively modified proteins, potentially disrupting cellular functions.
- While oxidative stress is implicated in muscle aging, specific oxidized protein targets remain unidentified.
Purpose of the Study:
- To identify specific oxidized proteins in human skeletal muscle associated with aging.
- To investigate the functional implications of protein carbonylation in the context of sarcopenia.
Main Methods:
- Proteomic analysis using two-dimensional gel electrophoresis.
- Immunodetection of carbonylated proteins in human rectus abdominis muscle biopsies from young and old donors.
Main Results:
- Seventeen protein spots showed increased carbonylation in older donors compared to younger donors.
- These identified proteins are crucial for cellular morphology, transport, muscle contraction, and energy metabolism.
- Oxidative modification of these proteins may impair key skeletal muscle functions.
Conclusions:
- Protein carbonylation is a significant molecular mechanism contributing to sarcopenia.
- The identified oxidized proteins represent potential targets for understanding and mitigating age-related muscle decline.
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