Abstract
Aging and sedentary life style are considered independent risk factors for many disorders. Under these conditions, accumulation of dysfunctional and damaged cellular proteins and organelles occurs, resulting in a cellular degeneration and cell death. Autophagy is a conserved recycling pathway responsible for the degradation, then turnover of cellular proteins and organelles. This process is a part of the molecular underpinnings by which exercise promotes healthy aging and mitigate age-related pathologies. Irisin is a myokine released during physical activity and acts as a link between muscles and other tissues and organs. Its main beneficial function is the change of subcutaneous and visceral adipose tissue into brown adipose tissue, with a consequential increase in thermogenesis. Irisin modulates metabolic processes, acting on glucose homeostasis, reduces systemic inflammation, maintains the balance between resorption and bone formation, and regulates the functioning of the nervous system. Recently, some of its pleiotropic and favorable properties have been attributed to autophagy induction, posing irisin as an important regulator of autophagy by exercise. This review article proposes to bring together for the first time the “state of the art” knowledge regarding the effects of irisin and autophagy. Furthermore, treatments on relation between exercise/myokines and autophagy have been also achieved.
Highlights
The myofibers are cells multinucleated that composed the skeletal muscle (SkM)
The myokines that have been described are included of cytokines, peptides, growth factors, and small organic acids. These molecules exert an effect on muscle function itself as well as on overall metabolism and comprise myostatin (MSTN), the small organic acid β-aminoisobutyric acid (BAIBA), meteorin-like (METRNL), myonectin, decorin, various interleukins (IL-4, IL-6, IL-7, IL-8, and IL-15), irisin, fibroblast growth factor-21 (FGF-21), brain-derived neurotrophic factor (BDNF), insulin-like growth factor-1 (IGF-1), leukemia inhibitory factor (LIF), and follistatin like protein-1 (FSTL-1) [28,36,37]
We focused on the pathological conditions in which irisin has been candidate as potential beneficial factor by autophagy induction
Summary
The myofibers are cells multinucleated that composed the skeletal muscle (SkM) These cells are responsible of the force generation by sarcomeres’ contraction and release several soluble factors (e.g., cytokines) exerting paracrine and endocrine functions. Autophagy is a catabolic process that has an essential role in cellular homeostasis, facilitating lysosomal degradation and recycling of intracellular misfolded proteins and injured organelles It is involved in the maintenance of various physiological responses and plays dual roles in inducing cytoprotection and cell death [8]. Abnormal regulation of autophagy may be an attribute to various pathologic conditions [9] and has been widely implicated in cancer, metabolic disorders, and neurodegenerative diseases, as well as muscle dystrophy It plays an important role in aging [10]. As irisin is a myokine induced after physical exercise, relation between exercise and autophagy as well as myokines and autophagy have been reviewed
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