Abstract
The incidence of skeletal muscle disorders and chronic diseases leading to skeletal muscle atrophy have been increasing worldwide due to sedentary lifestyle, poor quality of life and dietary modifications. This results in impaired metabolic homeostasis by increasing morbidity and in turn leading to increased mortality. In skeletal muscle, miRNAs regulate expression and secretion of myokines. Myokines, the bioactive molecules, influence miRNA expression profiles in muscle and distant tissues such as liver, adipose tissue, bone, brain, and immune cells. Dysregulation of myokines and miRNAs leads to obesity, insulin resistance, sarcopenia, neurodegenerative disorders, and cardiovascular diseases. Recent research has established the role of myokines and miRNAs as potential targets in combating skeletal muscle atrophy but no promising and effective treatment strategy has been developed yet. In this article, gene targets of miR-1 and miR-320 have been retrieved in Homo sapiens and Rattus norvegicus using miRDB 6.0, miRTarBase 10.0, TargetScan 8.0 and miRWalk 2.0 version databases, out of which all myokines have been screened and scrutinized. FNDC5 (irisin, a positive regulator of skeletal muscle mass) in hsa-miR-1 and hsa-miR-320; and MSTN (myostatin, a negative regulator of skeletal muscle mass) in hsa-miR-1 and rno-miR-320 were found to be the crucial targeting myokines. The miRNAs regulating the irisin and myostatin might play dynamic role in maintaining skeletal muscle homeostasis. Further, our own experimental validation of miRNA-myokine interactions has shown miRNAs might regulate levels of myokines under normal or stress conditions. While the role of myokines in regulating miRNA expression in skeletal muscle is still inadequately explored. Further investigation of miRNA–myokine network might help in identifying molecular targets for therapeutic interventions to improve clinical management of skeletal muscle disorders.
Keywords
Skeletal muscle atrophy, Skeletal muscle diseases, Myokine, miRNA, Therapeutics