miRNA‐23a/27a attenuates muscle atrophy and renal fibrosis through muscle‐kidney crosstalk

• Published in: Journal of cachexia, sarcopenia and muscle Vol. 9; no. 4; pp. 755 - 770
• Main Authors: Zhang, Aiqing, Li, Min, Wang, Bin, Klein, Janet D., Price, S. Russ, Wang, Xiaonan H.
• Format: Journal Article
• Language: English
• Published: Germany John Wiley & Sons, Inc 01.08.2018; John Wiley and Sons Inc; Wiley
• Subjects: Animals; Atrophy; Cloning; Crosstalk; Dependovirus - genetics; Diabetes; Diabetic nephropathy; Disease Models, Animal; Exosome; Fibrosis; Gene Expression Regulation; Genes; Genetic Vectors - genetics; Genomics; Insulin resistance; Insulin signalling; Kidney - metabolism; Kidney - pathology; Kidneys; Kinases; Mice; microRNA; MicroRNAs; MicroRNAs - genetics; Models, Biological; Molecular Imaging; Mortality; Muscular Atrophy - genetics; Muscular Atrophy - metabolism; Muscular Atrophy - pathology; Musculoskeletal system; Myostatin - metabolism; Original; Protein synthesis; Proteins; pSMAD2/3; Satellite Cells, Skeletal Muscle - metabolism; Signal Transduction; Transduction, Genetic; United States > US; pSMAD2/3; microRNA; Insulin signalling; Exosome; Crosstalk

Background The treatment of muscle wasting is accompanied by benefits in other organs, possibly resulting from muscle–organ crosstalk. However, how the muscle communicates with these organs is less understood. Two microRNAs (miRs), miR‐23a and miR‐27a, are located together in a gene cluster and regu...