Modulatory Effect of Myokines on Reactive Oxygen Species in Ischemia/Reperfusion

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.

Notoginseng Triterpenes Inhibited Autophagy in Random Flaps via the Beclin-1/VPS34/LC3 Signaling Pathway to Improve Tissue Survival

“…Reactive oxygen species (ROS) mainly cause the damage of microvessels and parenchymal organs during ischemic tissue reperfusion. The synthesis ability of antioxidant enzymes, which can scavenge free radicals, is impaired in the ischemic tissue, thus aggravating the damage of free radicals to ischemic reperfusion tissue (Neeff et al, 2012;Sun et al, 2014;Szabó et al, 2020). SOD can protect the tissue from ischemia and reperfusion by scavenging free radicals (Ambrosio et al, 1987;Galiñanes et al, 1992;Chen et al, 1996;Zhao et al, 2018).…”

Mechanisms of neuronal cell death in ischemic stroke and their therapeutic implications

“…46 Reactive oxygen species-mediated apoptosis When blood flow is restored after cerebral ischemia, a large amount of reactive oxygen species (ROS) is produced, which may be one of the causes of neuronal ischemia/reperfusion (I/R) injury. 47 Neuronal cell damage by ROS may occur in association with apoptosis. For example, ROS can damage the plasma membrane, resulting in loss of membrane integrity.…”

Effects of Intermittent Hypoxia on Cytokine Expression Involved in Insulin Resistance

“…Many studies have shown that inflammation associated with I/R injury can exacerbate myocardial damage [ 96 ], which may cause a condition experimentally similar to IH. On the basis of these studies [ 97 ], we suspected that IH had a direct effect on myokine secretion and conducted the following experiments. We investigated the changes in myokine levels and their regulation mechanisms by IH [ 19 ].…”