Autophagy in Muscle Regeneration: Mechanisms, Targets, and Therapeutic Perspective.

Int J Mol Sci

Department of Emergency, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

Published: November 2024

Autophagy maintains the stability of eukaryotic cells by degrading unwanted components and recycling nutrients and plays a pivotal role in muscle regeneration by regulating the quiescence, activation, and differentiation of satellite cells. Effective muscle regeneration is vital for maintaining muscle health and homeostasis. However, under certain disease conditions, such as aging, muscle regeneration can fail due to dysfunctional satellite cells. Dysregulated autophagy may limit satellite cell self-renewal, hinder differentiation, and increase susceptibility to apoptosis, thereby impeding muscle regeneration. This review explores the critical role of autophagy in muscle regeneration, emphasizing its interplay with apoptosis and recent advances in autophagy research related to diseases characterized by impaired muscle regeneration. Additionally, we discuss new approaches involving autophagy regulation to promote macrophage polarization, enhancing muscle regeneration. We suggest that utilizing cell therapy and biomaterials to modulate autophagy could be a promising strategy for supporting muscle regeneration. We hope that this review will provide new insights into the treatment of muscle diseases and promote muscle regeneration.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11593790PMC
http://dx.doi.org/10.3390/ijms252211901DOI Listing

Publication Analysis

Top Keywords

muscle regeneration
40
muscle
11
regeneration
10
autophagy muscle
8
satellite cells
8
autophagy
7
regeneration mechanisms
4
mechanisms targets
4
targets therapeutic
4
therapeutic perspective
4

Similar Publications

Background: Rupture of extensor pollicis longus tendon (EPL) is a known complication following a distal radius fracture (DRF). Although the precise mechanisms behind these ruptures remain unclear, vascular impairment is thought to play a significant role. Additionally, the impact of an EPL rupture on microstructure of the tendon and muscle is not well understood, but such information could be important in guiding treatment strategies.

View Article and Find Full Text PDF

IL-6 Promotes Muscle Atrophy by Increasing Ubiquitin-Proteasome Degradation of Muscle Regeneration Factors After Cerebral Infarction in Rats.

Neuromolecular Med

January 2025

Department of Rehabilitation Medicine, The Affiliated Jiangning Hospital of Nanjing Medical University, No. 168 Gushan Road, Dongshan Street, Jiangning District, Nanjing, 211199, Jiangsu, China.

Muscle atrophy in pathological or diseased muscles arises from an imbalance between protein synthesis and degradation. Elevated levels of interleukin-6 (IL-6) are a hallmark of ischemic stroke and have been associated with muscle atrophy in certain pathological contexts. However, the mechanisms by which IL-6 induces muscle atrophy in the context of stroke remain unclear.

View Article and Find Full Text PDF

The negative effects of particulate matter up to 2.5 μm in diameter (PM) and their mediating mechanisms have been studied in various tissues. However, little is known about the mechanism and long-term tracking underlying the sex-dependent effects of PM on skeletal muscle system modulation.

View Article and Find Full Text PDF

Skeletal muscle dysfunction (SMD), one of the extrapulmonary complications in patients with chronic obstructive pulmonary disease (COPD), considerably influences patient prognosis. Mitochondria regulates their dynamic networks through a mitochondria quality control (MQC) mechanism, involving mitochondrial biogenesis, mitochondrial dynamics, and mitophagy. The MQC is crucial for mitochondrial homeostasis and health, and disruption of it can lead to mitochondrial damage, which is a key factor in the structural and functional impairment of skeletal muscle in COPD.

View Article and Find Full Text PDF

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

Alzheimer's Center at Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.

Background: FDA-approved carbonic anhydrase inhibitors (CAIs) have been shown to attenuate Aβ pathology, neurodegeneration, and cerebrovascular dysfunction in models of Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA), suggesting a key role for CAs as a novel and previously unexplored target for AD therapy. Amyloid β accumulation severely impairs the cerebral neuro-signaling pathway with a progressive loss in neurotrophic factors (NTFs, i.e.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!