Abstract
There is a growing body of evidence showing the importance of physical activity against acute ischemic events in various organs. Ischemia/reperfusion injury (I/R) is characterized by tissue damage as a result of restriction and subsequent restoration of blood supply to an organ. Oxidative stress due to increased reactive oxygen species formation and/or insufficient antioxidant defense is considered to play an important role in I/R. Physical activity not only decreases the general risk factors for ischemia but also confers direct anti-ischemic protection via myokine production. Myokines are skeletal muscle-derived cytokines, representing multifunctional communication channels between the contracting skeletal muscle and other organs through an endocrine manner. In this review, we discuss the most prominent members of the myokines (i.e., brain-derived neurotrophic factor (BDNF), cathepsin B, decorin, fibroblast growth factors-2 and -21, follistatin, follistatin-like, insulin-like growth factor-1; interleukin-6, interleukin-7, interleukin-15, irisin, leukemia inhibitory factor, meteorin-like, myonectin, musclin, myostatin, and osteoglycin) with a particular interest in their potential influence on reactive oxygen and nitrogen species formation or antioxidant capacity. A better understanding of the mechanism of action of myokines and particularly their participation in the regulation of oxidative stress may widen their possible therapeutic use and, thereby, may support the fight against I/R.
Highlights
Tissue damage caused by ischemia/reperfusion (I/R) injury is presented in various clinical manifestations and is considered to be a leading cause of death all over the world
We introduce the effects of the different myokines and the current position on their possible relation to the oxidative stress modulation in the context of I/R
Fibroblast growth factor-21 (FGF-21) transcription is highly regulated by activating transcription factor 4 (ATF-4) and CCAAT enhancer-binding protein homologous protein (CHOP), two important regulators of redox homeostasis and endoplasmic reticulum (ER)-stress [140]
Summary
Tissue damage caused by ischemia/reperfusion (I/R) injury is presented in various clinical manifestations (e.g., myocardial infarction, stroke, peripheral arterial disease, ischemic nephropathy, etc.) and is considered to be a leading cause of death all over the world. IL-6 increased the activation of STAT3, expression of SOD-2, and decreased superoxide anion production [44] These mechanisms were in casual relation to the cytoprotection against OGD and in vivo ischemic stroke [44]. COX-2: cyclooxygenase-2, DHE: Dihydroethidium assay, GSH: glutathione, HO: heme oxygenase, HSP70: heat shock protein 70, ip.: intraperitoneally, icv.: intracerebroventricularly, MDA: malondialdehyde, SOD-2: MnSOD, NF-kB: nuclear factor kappa-light-chain-enhancer of activated B cells, NOS-1, NOS-2, and NOS-3: neuronal/inducible/endothelial nitric oxide synthase, O2 − : superoxide anion, OGD: oxygen-glucose deprivation, sI/R: simulated ischemia/reperfusion, SOD: superoxide dismutase, ↑ and ↓indicate increase and decrease, respectively;. GSH content by the modulation of glutathione-related enzymes [48]
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