Mitochondrial dynamics, quality control and miRNA regulation in skeletal muscle: implications for obesity and related metabolic disease

The western dietary habits and sedentary lifestyle largely contributes to the growing epidemic of obesity. Mitochondria are at the front line of cellular energy homoeostasis and are implicated in the pathophysiology of obesity and obesity-related metabolic disease. In recent years, novel aspects in the regulation of mitochondrial metabolism, such as mitochondrial dynamics, mitochondrial protein quality control and post-transcriptional regulation of genes coding for mitochondrial proteins, have emerged. In this review, we discuss the recent findings concerning the dysregulation of these processes in skeletal muscle in obesogenic conditions. * ClpXP, : ATP-dependent caseinolytic mitochondrial matrix protease complex; Drp-1, : dynamin-related protein 1; ETC, : electron transport chain; Fis1, : fission protein 1; FOXJ3, : Forkhead Box J3; IMS, : mitochondrial intermembrane space; LC3, : microtubule-associated protein 1A/1B-light chain 3 proteins; lncRNA, : long non-coding RNA; LonP, : Lon protease; mff, : mitochondrial fission factor; Mfn-1, : mitofusin-1; Mfn-2, : mitofusin-2; MID49/51, : mitochondrial dynamics proteins of 49 and 51 kDa; Mrps-5, : mitochondrial ribosomal protein subunit 5; mtDNA, : mitochondrial DNA; MTS, : N-terminal matrix-sequence; mtTFA, : mitochondrial transcription factor A; mtUPR, : mitochondrial unfolded protein response; Opa1, : optic atrophy 1; PARP-2, : poly(ADP-ribosyl) transferase-like 2 protein; PBMC, : peripheral blood mononuclear cell; PINK1, : PTEN-induced putative kinase 1; RISC, : RNA induced silencing complex; ROS, : reactive oxygen species; T2DM, : type 2 diabetes mellitus; UPR, : unfolded protein response