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Скачать или смотреть Arginase-II Deficiency Slows Skeletal Muscle Aging in Mice | Aging-US

  • Aging-US
  • 2025-01-20
  • 70
Arginase-II Deficiency Slows Skeletal Muscle Aging in Mice | Aging-US
agingarginase-IIcellular senescencefibrosisphysical activityskeletal muscle
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Описание к видео Arginase-II Deficiency Slows Skeletal Muscle Aging in Mice | Aging-US

Aging-US #published this #trending research paper on December 12, 2024, in Volume 16, Issue 22, entitled "Arginase-II gene deficiency reduces skeletal muscle aging in mice" by researchers from the Department of Endocrinology, Metabolism, and Cardiovascular System, Faculty of Science and Medicine, University of Fribourg, Fribourg 1700, Switzerland; Department of Biology, Faculty of Science and Medicine, University of Fribourg, Fribourg 1700, Switzerland. ‪@universitedeFribourgFreiburg‬
#aging #skeletalmuscle #physicalactivity #fibrosis #research #openaccess #openscience #peerreviewed #journalpublication #publishing #meded

DOI - https://doi.org/10.18632/aging.206173

Corresponding authors - Andrea Brenna - [email protected], and Zhihong Yang - [email protected]

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.

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Keywords - aging, arginase-II, cellular senescence, fibrosis, physical activity, skeletal muscle

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

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