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Role of Actin-Binding Proteins in Skeletal Myogenesis

Title
Role of Actin-Binding Proteins in Skeletal Myogenesis
Author(s)
Nguyen, Mai ThiDash, RajuJeong, KyuhoLee, Wan
Issued Date
2023-11
Citation
Cells, v.12, no.21
Type
Article
Author Keywords
actin-binding proteinsactin dynamicsmyogenesisdifferentiationproliferationnon-coding RNA
Keywords
SERUM RESPONSE FACTORALDRICH-SYNDROME PROTEINMUSCLE-CELL FUSIONN-WASPTRANSCRIPTION FACTORMYOBLAST FUSIONARP2/3 COMPLEXFILAMIN-CPHOSPHATIDYLINOSITOL 3-KINASETHIN-FILAMENTS
ISSN
2073-4409
Abstract
Maintenance of skeletal muscle quantity and quality is essential to ensure various vital functions of the body. Muscle homeostasis is regulated by multiple cytoskeletal proteins and myogenic transcriptional programs responding to endogenous and exogenous signals influencing cell structure and function. Since actin is an essential component in cytoskeleton dynamics, actin-binding proteins (ABPs) have been recognized as crucial players in skeletal muscle health and diseases. Hence, dysregulation of ABPs leads to muscle atrophy characterized by loss of mass, strength, quality, and capacity for regeneration. This comprehensive review summarizes the recent studies that have unveiled the role of ABPs in actin cytoskeletal dynamics, with a particular focus on skeletal myogenesis and diseases. This provides insight into the molecular mechanisms that regulate skeletal myogenesis via ABPs as well as research avenues to identify potential therapeutic targets. Moreover, this review explores the implications of non-coding RNAs (ncRNAs) targeting ABPs in skeletal myogenesis and disorders based on recent achievements in ncRNA research. The studies presented here will enhance our understanding of the functional significance of ABPs and mechanotransduction-derived myogenic regulatory mechanisms. Furthermore, revealing how ncRNAs regulate ABPs will allow diverse therapeutic approaches for skeletal muscle disorders to be developed. © 2023 by the authors.
URI
http://hdl.handle.net/20.500.11750/46689
DOI
10.3390/cells12212523
Publisher
MDPI
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