Abstract
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.
Highlights
Cachexia is a complex metabolic condition accompanied by progressive bodyweight loss, skeletal muscle atrophy, and decreased muscle strength
Cachexia is common in patients with certain cancers and other diseases in the advanced stages, such as patients with intensive care unit (ICU)-acquired (Garros et al, 2017) weakness or chronic obstructive pulmonary disease (COPD) (Man et al, 2009), chronic kidney disease (CKD) (Zhang et al, 2019), and heart failure (Anker et al, 1997)
In experiments in L6 myocytes, apoptosis was accelerated after induction of miR-628 expression, and the protein levels of Insulin receptor substrate 1 (IRS1) and p-Akt, involved in the IRS1/Akt/FoxO pathway, TABLE 2 | Functional miRNAs involved in skeletal muscle wasting in human cachexia
Summary
Cachexia is a complex metabolic condition accompanied by progressive bodyweight loss, skeletal muscle atrophy, and decreased muscle strength. In experiments in L6 myocytes, apoptosis was accelerated after induction of miR-628 expression, and the protein levels of IRS1 and p-Akt, involved in the IRS1/Akt/FoxO pathway, TABLE 2 | Functional miRNAs involved in skeletal muscle wasting in human cachexia.
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
