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Updated: Aug 5, 2026
Myo-mechanical Analysis of Isolated Skeletal Muscle
Published on: February 22, 2011
Arginase-II gene deficiency reduces skeletal muscle aging in mice
Matteo Caretti1, Duilio Michele Potenza1, Guillaume Ajalbert1
1Department of Endocrinology, Metabolism, and Cardiovascular System, Faculty of Science and Medicine, University of Fribourg, Fribourg 1700, Switzerland.
Abstract:
Age-associated sarcopenia decreases mobility and is promoted by cell senescence, inflammation, and fibrosis. The mitochondrial enzyme arginase-II (Arg-II) plays a causal role in aging and age-associated diseases. Therefore, we aim to explore the role of Arg-II in age-associated decline of physical activity and skeletal muscle aging in a mouse model. Young (4-6 months) and old (20-24 months) wild-type (wt) mice and mice deficient in arg-ii (arg-ii-/-) of both sexes are investigated. We demonstrate a decreased physical performance of old wt mice, which is partially prevented in arg-ii-/- animals, particularly in males. The improved phenotype of arg-ii-/- mice in aging is associated with reduced sarcopenia, cellular senescence, inflammation, and fibrosis, whereas age-associated decline of microvascular endothelial cell density, satellite cell numbers, and muscle fiber types in skeletal muscle is prevented in arg-ii-/- mice. Finally, we demonstrate an increased arg-ii gene expression level in aging skeletal muscle and found Arg-II protein expression in endothelial cells and fibroblasts, but not in skeletal muscle fibers, macrophages, and satellite cells. Our results suggest that increased Arg-II in non-skeletal muscle cells promotes age-associated sarcopenia, particularly in male mice.
Insights
Mitochondrial enzyme arginase-II (Arg-II) contributes to age-related muscle loss (sarcopenia). Reducing Arg-II in mice improved physical function and reduced aging markers, suggesting a therapeutic target.
Area of Science:
- Gerontology
- Mitochondrial Biology
- Skeletal Muscle Physiology
Background:
- Age-associated sarcopenia impairs mobility and is linked to cellular senescence, inflammation, and fibrosis.
- The mitochondrial enzyme arginase-II (Arg-II) is implicated in aging processes and age-related diseases.
Purpose of the Study:
- To investigate the role of Arg-II in age-related decline of physical activity and skeletal muscle aging.
- To determine if Arg-II deficiency mitigates age-associated skeletal muscle dysfunction in a mouse model.
Main Methods:
- Comparison of young and old wild-type mice with age-matched mice deficient in arginase-II (arg-ii) of both sexes.
- Assessment of physical performance, sarcopenia markers, cellular senescence, inflammation, fibrosis, microvascular density, satellite cell numbers, and muscle fiber types.
- Analysis of arg-II gene and protein expression in aging skeletal muscle and associated cell types.
Main Results:
- Old wild-type mice exhibited decreased physical performance, which was partially preserved in arg-ii deficient mice, especially males.
- Arg-II deficiency reduced sarcopenia, cellular senescence, inflammation, and fibrosis in aging mice.
- Age-associated decline in microvascular endothelial cell density, satellite cell numbers, and muscle fiber types was prevented in arg-ii mice.
- Increased arg-II gene expression was observed in aging skeletal muscle, with Arg-II protein localized to endothelial cells and fibroblasts.
Conclusions:
- Increased Arg-II in non-skeletal muscle cells contributes to age-associated sarcopenia, particularly in males.
- Arg-II deficiency ameliorates age-related skeletal muscle decline and improves physical function.
- Targeting Arg-II presents a potential strategy for combating age-related sarcopenia.
