Irisin, Exercise, and COVID-19

Abstract

Muscle and adipose tissue produce irisin during exercise. Irisin is thermogenic adipomyokine, improves glucose and lipid metabolism, and ameliorates the effects of obesity-driven inflammation, metabolic syndrome, and diabetes. In addition, exercise-induced irisin activates anti-inflammatory pathways and may play an essential role in improving the outcomes of inflammatory conditions, such as coronavirus disease (COVID-19). COVID-19 infection can activate different intracellular receptors and modulate various pathways during the course of the disease. The cytokine release storm (CRS) produced is significant because it promotes the context for systemic inflammation, which increases the risk of mortality in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV2). In addition, viral infection and the resulting organ damage may stimulate the mitogen-activated protein kinase(MAPK) and toll-like receptor 4 (TLR4)/toll interleukin receptor (TIR)-domain-containing adaptor (MyD88) pathways while negatively modulating the AMP-activated protein kinase (AMPK) pathway, leading to increased inflammatory cytokine production. Exercise-induced irisin may counteract this inflammatory modulation by decreasing cytokine production. Consequently, increased irisin levels, as found in healthy patients, may favor a better prognosis in patients with SARS-CoV2. This review aims to explore the molecular mechanisms underlying the anti-inflammatory properties of irisin in mitigating CRS and preventing severe outcomes due to infection with SARS-CoV2.

Recombinant irisin enhances the extracellular matrix formation, remodeling potential, and differentiation of human periodontal ligament cells cultured in 3D

“…The IPA analysis also identified several important signaling pathways involved upon irisin exposure. Interestingly, we found that coronavirus replication pathway was activated upon irisin treatment, though irisin has been reported to counteract the adverse effects of COVID‐19 during the various disease stages, 47 no research up to date has studied its role on coronavirus‐infected hPDL cells yet. The actin cytoskeleton rearrangement is key to both withstanding extracellular mechanical strain and intracellular structural support, and inhibition of actin cytoskeleton leads to down regulation of collagen type I, 48 the activation of actin cytoskeleton signaling may suggest reinforcement of ECM by irisin.…”

Cellular Metabolism: A Fundamental Component of Degeneration in the Nervous System

“…If one has greater than a high school education, the risk decreases to seven and onehalf percent. Additional risk factors for developing complications of DM consist of tobacco consumption, hypertension, exercise, elevated serum cholesterol, and obesity [6][7][8][9][10][11][12][13]. In regard to obesity, increased body weight leads to impaired glucose tolerance that results in DM progression [14][15][16][17][18][19][20][21][22][23][24].…”

Cognitive Impairment in Multiple Sclerosis

“…mTOR can modulate insulin physiology in neurodegenerative studies to increase survival of astrocytes [429], block hyperglycemic endothelial cell injury [430], and preserve metabolic regulation [431]. As a component of the mTOR pathway, the AMP-activated protein kinase (AMPK) modulates cellular metabolism [106,169,198,237,378,381,382,394,432,433], and the activation of AMPK reduces cognitive loss in studies of DM and AD [434,435], removes cerebral Aβ [436] and tau [437], limits Aβ neurotoxicity [392], diminishes long-term inflammation in in the nervous system [10,71,438,439], and fosters pathways for healthy aging [6,440,441].…”