Skeletal Muscle Atrophy in Health and Disease: From Molecular Mechanisms to Therapeutic Opportunities

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 15 October 2024 | Viewed by 1251

Special Issue Editor

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Guest Editor
1. Department of Biomedical Sciences, University of Padua, Padua, Italy
2. Myology Center (CIR-Myo), University of Padua, Padua, Italy
Interests: neuromuscular plasticity; muscle contraction; disuse; aging
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Special Issue Information

Dear Colleagues,

Skeletal muscle atrophy is a condition common to disuse, immobilization, injury, trauma, disease and aging. Atrophy can be an extremely fast process that can be detected after just 3 days of muscle unloading in healthy humans. Many clinical conditions involving inflammation and oxidative stress exacerbate muscle wasting and, when associated with the loss of muscle mass occurring with ageing (sarcopenia), lead to frailty and loss of independence. Yet, the molecular mechanisms responsible for muscle atrophy in many neuromuscular disorders, such as amyotrophic lateral sclerosis (ALS), spinal muscle atrophy (SMA), multiple sclerosis (MS), muscular dystrophy (MD), myasthenia gravis (MG), myopathies, neuropathies, etc., as well as in aging and inactivity, are to be fully understood. The paucity of knowledge also exists on the efficacy of the physical, nutritional and pharmacological intervention on the recovery of muscle loss in most neuromuscular disorders and aging. Even in healthy young adults, chronic inactivity seems to trigger neuropathic processes causing instability of the neuromuscular junction, axonal damage and denervation/reinnervation of muscle fibres.

This Special Issue will review the current knowledge on the mechanisms of muscle atrophy with disuse, inactivity, aging and with some of the most relevant neuromuscular disorders and discuss the effect of conventional but also innovative therapeutic interventions in the prevention/recovery of muscle mass and strength loss associated with these conditions.

Prof. Dr. Marco Vincenzo Narici
Guest Editor

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  • muscle atrophy
  • inactivity
  • ageing
  • sarcopenia
  • neuromuscular disorders

Published Papers (1 paper)

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14 pages, 4353 KiB  
Silk Peptide Ameliorates Sarcopenia through the Regulation of Akt/mTOR/FoxO3a Signaling Pathways and the Inhibition of Low-Grade Chronic Inflammation in Aged Mice
by Hyun-Ji Oh, Heegu Jin, Jeong-Yong Lee and Boo-Yong Lee
Cells 2023, 12(18), 2257; - 12 Sep 2023
Cited by 1 | Viewed by 1006
As populations around the world age, interest in healthy aging is growing. One of the first physical changes that occurs with aging is the loss of muscle mass and strength, termed sarcopenia. Sarcopenia limits the activity of older people, reduces their quality of [...] Read more.
As populations around the world age, interest in healthy aging is growing. One of the first physical changes that occurs with aging is the loss of muscle mass and strength, termed sarcopenia. Sarcopenia limits the activity of older people, reduces their quality of life, and increases the likelihood of their developing disease. In the present study, we aimed to evaluate the effects of the ingestion of acid-hydrolyzed silk peptide (SP) on the muscle mass and strength of mice of >22 months of age with naturally occurring sarcopenia, and to identify the mechanisms involved. The daily administration of SP for 8 weeks increased the activation of the Akt/mTOR/FoxO3a signaling pathways and increased the muscle mass and strength of the old mice. In addition, SP inhibited oxidative stress and inflammation in muscle, which are direct causes of sarcopenia. Therefore, SP represents a promising potential treatment for sarcopenia that may improve the healthy lifespan and quality of life of older people. Full article
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