MicroRNAs in muscle wasting

Suzuki, Tsuyoshi; Springer, Jochen

doi:10.1002/jcsm.12384

Cited by 13 publications

(11 citation statements)

References 41 publications

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“…The roles of miRNAs in skeletal muscle in certain diseases have been well described in different muscular atrophy models, and in recent years, the involvement of miRNAs in regulating muscular atrophy in cachexia has been confirmed. These miRNAs could serve not only as biomarkers for muscle status and wasting but also as biomarkers to monitor muscle regeneration and therapy effects (Suzuki and Springer, 2018). miRNAs associated with muscular atrophy in disease are expected to be identified in the future, and they may function by many different mechanisms.…”

Section: Discussionmentioning

confidence: 99%

Regulation of Skeletal Muscle Atrophy in Cachexia by MicroRNAs and Long Non-coding RNAs

Chen

Liu

Jiang

et al. 2020

Front. Cell Dev. Biol.

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Skeletal muscle atrophy is a common complication of cachexia, characterized by progressive bodyweight loss and decreased muscle strength, and it significantly increases the risks of morbidity and mortality in the population with atrophy. Numerous complications associated with decreased muscle function can activate catabolism, reduce anabolism, and impair muscle regeneration, leading to muscle wasting. microRNAs (miRNAs) and long non-coding RNAs (lncRNAs), types of non-coding RNAs, are important for regulation of skeletal muscle development. Few studies have specifically identified the roles of miRNAs and lncRNAs in cellular or animal models of muscular atrophy during cachexia, and the pathogenesis of skeletal muscle wasting in cachexia is not entirely understood. To develop potential approaches to improve skeletal muscle mass, strength, and function, a more comprehensive understanding of the known key pathophysiological processes leading to muscular atrophy is needed. In this review, we summarize the known miRNAs, lncRNAs, and corresponding signaling pathways involved in regulating skeletal muscle atrophy in cachexia and other diseases. A comprehensive understanding of the functions and mechanisms of miRNAs and lncRNAs during skeletal muscle wasting in cachexia and other diseases will, therefore, promote therapeutic treatments for muscle atrophy.

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Section: Discussionmentioning

confidence: 99%

Regulation of Skeletal Muscle Atrophy in Cachexia by MicroRNAs and Long Non-coding RNAs

Chen

Liu

Jiang

et al. 2020

Front. Cell Dev. Biol.

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“…These regulators of gene expression have not been extensively described in exercised skeletal muscle during conditions of wasting, but existing evidence supports that they can influence muscle development, hypertrophy, atrophy, and wasting (56)(57)(58)(59). We highlight and summarize well-known epigenetic regulators below and direct the reader to resources that cover these factors in depth (60)(61)(62)(63)(64)(65). miRNAs are short $22 nucleotide, noncoding RNAs which bind to the 3 0 UTR of target mRNA to inhibit or impair translation.…”

Section: Epigeneticsmentioning

confidence: 99%

“…They have been implicated in many aspects of skeletal muscle formation, development, health, and responses to exercise (66). Skeletal muscle produces tissue-specific miRNAs known as myomiRs (61,66). The first myomiRs identified include miR-1, miR-133a/b, and miR-206.…”

Section: Epigeneticsmentioning

confidence: 99%

Mechanisms of exercise as a preventative measure to muscle wasting

Graham

Lavin

O’Bryan

et al. 2021

American Journal of Physiology-Cell Physiology

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Skeletal muscle is the most abundant tissue in healthy individuals and it has important roles in health beyond voluntary movement. The overall mass and energy requirements of skeletal muscle require it to be metabolically active and flexible to multiple energy substrates. The tissue has evolved to be largely load-dependent and it readily adapts in a number of positive ways to repetitive overload, such as various forms of exercise training. However, unloading from extended bed rest and/or metabolic derangements in response to trauma, acute illness, or severe pathology, commonly result in rapid muscle wasting. Declines in muscle mass contribute to multi-morbidity, reduce function and exert a substantial, negative impact on quality of life. The principal mechanisms controlling muscle mass have been well-described and these cellular processes are intricately regulated by exercise. Accordingly, exercise has shown great promise and efficacy in preventing or slowing muscle wasting through changes in molecular physiology, organelle function, cell signaling pathways and epigenetic regulation. In this review we focus on the role of exercise in altering the molecular landscape of skeletal muscle in a manner that improves or maintains its health and function in the presence of unloading or disease.

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“…The role of myomiRs in the regulation of muscle homeostasis, development and functionality has been extensively characterized (Horak et al, 2016;Sjögren et al, 2017). Moreover, deregulation of their expression resulted to be associated with muscle atrophy, one of the main hallmark of cancer-associated cachexia (Suzuki and Springer, 2018).…”

Section: Are Skeletal Muscle Micrornas Potential Biomarkers For Cancementioning

confidence: 99%