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骨胳肌萎缩的表观遗传控制。

Epigenetic control of skeletal muscle atrophy.

机构信息

Key Laboratory of Neuroregeneration of Jiangsu and Ministry of Education, Co-Innovation Center of Neuroregeneration, NMPA Key Laboratory for Research and Evaluation of Tissue Engineering Technology Products, Nantong University, Nantong, 26001, China.

Department of Prenatal Screening and Diagnosis Center, Affiliated Maternity and Child Health Care Hospital of Nantong University, Nantong, 226001, China.

出版信息

Cell Mol Biol Lett. 2024 Jul 8;29(1):99. doi: 10.1186/s11658-024-00618-1.


DOI:10.1186/s11658-024-00618-1
PMID:38978023
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11229277/
Abstract

Skeletal muscular atrophy is a complex disease involving a large number of gene expression regulatory networks and various biological processes. Despite extensive research on this topic, its underlying mechanisms remain elusive, and effective therapeutic approaches are yet to be established. Recent studies have shown that epigenetics play an important role in regulating skeletal muscle atrophy, influencing the expression of numerous genes associated with this condition through the addition or removal of certain chemical modifications at the molecular level. This review article comprehensively summarizes the different types of modifications to DNA, histones, RNA, and their known regulators. We also discuss how epigenetic modifications change during the process of skeletal muscle atrophy, the molecular mechanisms by which epigenetic regulatory proteins control skeletal muscle atrophy, and assess their translational potential. The role of epigenetics on muscle stem cells is also highlighted. In addition, we propose that alternative splicing interacts with epigenetic mechanisms to regulate skeletal muscle mass, offering a novel perspective that enhances our understanding of epigenetic inheritance's role and the regulatory network governing skeletal muscle atrophy. Collectively, advancements in the understanding of epigenetic mechanisms provide invaluable insights into the study of skeletal muscle atrophy. Moreover, this knowledge paves the way for identifying new avenues for the development of more effective therapeutic strategies and pharmaceutical interventions.

摘要

骨骼肌萎缩是一种复杂的疾病,涉及大量基因表达调控网络和各种生物学过程。尽管对此进行了广泛的研究,但它的潜在机制仍难以捉摸,尚未建立有效的治疗方法。最近的研究表明,表观遗传学在调节骨骼肌萎缩中起着重要作用,通过在分子水平上添加或去除某些化学修饰,影响与该疾病相关的许多基因的表达。这篇综述文章全面总结了 DNA、组蛋白、RNA 及其已知调节剂的不同修饰类型。我们还讨论了表观遗传修饰如何在骨骼肌萎缩过程中发生变化,表观遗传调节蛋白控制骨骼肌萎缩的分子机制,并评估其转化潜力。此外,还强调了表观遗传学在肌肉干细胞中的作用。我们还提出,选择性剪接与表观遗传机制相互作用,以调节骨骼肌质量,提供了一个新的视角,增强了我们对表观遗传遗传作用和调控骨骼肌萎缩的网络的理解。总之,对表观遗传机制的理解的进步为研究骨骼肌萎缩提供了宝贵的见解。此外,这一知识为确定开发更有效的治疗策略和药物干预的新途径铺平了道路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef9c/11229277/5702c25644d9/11658_2024_618_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef9c/11229277/09e99b1912e1/11658_2024_618_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef9c/11229277/9fe065e8bb08/11658_2024_618_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef9c/11229277/5702c25644d9/11658_2024_618_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef9c/11229277/09e99b1912e1/11658_2024_618_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef9c/11229277/9fe065e8bb08/11658_2024_618_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef9c/11229277/5702c25644d9/11658_2024_618_Fig3_HTML.jpg

相似文献

[1]
Epigenetic control of skeletal muscle atrophy.

Cell Mol Biol Lett. 2024-7-8

[2]
Epigenetics of Skeletal Muscle Atrophy.

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[3]
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[4]
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Mol Biol Rep. 2023-7

[5]
Alternative splicing transitions associate with emerging atrophy phenotype during denervation-induced skeletal muscle atrophy.

J Cell Physiol. 2021-6

[6]
Altered m6A RNA methylation governs denervation-induced muscle atrophy by regulating ubiquitin proteasome pathway.

J Transl Med. 2023-11-23

[7]
One week, but not 12 hours, of cast immobilization alters promotor DNA methylation patterns in the nNOS gene in mouse skeletal muscle.

J Physiol. 2019-10-9

[8]
Histone deacetylase 6 is a FoxO transcription factor-dependent effector in skeletal muscle atrophy.

J Biol Chem. 2015-2-13

[9]
Coordinated Actions of MicroRNAs with other Epigenetic Factors Regulate Skeletal Muscle Development and Adaptation.

Int J Mol Sci. 2017-4-15

[10]
DNA methyltransferase 3a and mitogen-activated protein kinase signaling regulate the expression of fibroblast growth factor-inducible 14 (Fn14) during denervation-induced skeletal muscle atrophy.

J Biol Chem. 2014-7-18

引用本文的文献

[1]
Developmental Programming and Postnatal Modulations of Muscle Development in Ruminants.

Biology (Basel). 2025-7-24

[2]
Taurine Attenuates Disuse Muscle Atrophy Through Modulation of the xCT-GSH-GPX4 and AMPK-ACC-ACSL4 Pathways.

Antioxidants (Basel). 2025-7-10

[3]
Exploration of Pathogenesis and Cutting-Edge Treatment Strategies of Sarcopenia: A Narrative Review.

Clin Interv Aging. 2025-5-23

[4]
Analysis of the mechanism of skeletal muscle atrophy from the pathway of decreased protein synthesis.

Front Physiol. 2025-4-25

[5]
The Functions and Regulatory Mechanisms of Histone Modifications in Skeletal Muscle Development and Disease.

Int J Mol Sci. 2025-4-12

[6]
Dietary advanced glycation end-products exacerbate sarcopenia onset by activating apoptosis through PRMT1-mediated CRTC3 arginine methylation.

Cell Mol Life Sci. 2025-4-7

[7]
Stem cell therapy: A promising therapeutic approach for skeletal muscle atrophy.

World J Stem Cells. 2025-2-26

[8]
Liposome-Enabled Nanomaterials for Muscle Regeneration.

Small Methods. 2025-2-18

[9]
Ferroptosis and Its Potential Role in the Physiopathology of Skeletal Muscle Atrophy.

Int J Mol Sci. 2024-11-20

本文引用的文献

[1]
Roles of Myokines and Muscle-Derived Extracellular Vesicles in Musculoskeletal Deterioration under Disuse Conditions.

Metabolites. 2024-1-26

[2]
The epigenetic regulatory effect of histone acetylation and deacetylation on skeletal muscle metabolism-a review.

Front Physiol. 2023-12-8

[3]
Altered m6A RNA methylation governs denervation-induced muscle atrophy by regulating ubiquitin proteasome pathway.

J Transl Med. 2023-11-23

[4]
DNA hypomethylation characterizes genes encoding tissue-dominant functional proteins in liver and skeletal muscle.

Sci Rep. 2023-11-5

[5]
Epitranscriptomics as a New Layer of Regulation of Gene Expression in Skeletal Muscle: Known Functions and Future Perspectives.

Int J Mol Sci. 2023-10-13

[6]
Ythdf2-mediated STK11 mRNA decay supports myogenesis by inhibiting the AMPK/mTOR pathway.

Int J Biol Macromol. 2024-1

[7]
Reprogramming of cis-regulatory networks during skeletal muscle atrophy in male mice.

Nat Commun. 2023-10-18

[8]
Crosstalk between m6A modification and alternative splicing during cancer progression.

Clin Transl Med. 2023-10

[9]
Sodium butyrate does not protect spinal motor neurons from AMPA-induced excitotoxic degeneration in vivo.

Dis Model Mech. 2023-10-1

[10]
Regulation of alternative splicing: Functional interplay with epigenetic modifications and its implication to cancer.

Wiley Interdiscip Rev RNA. 2023-9-12

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