The potential molecular implications of adiponectin in the evolution of SARS-CoV-2: Inbuilt tendency

[Display omitted] Adiponectin (APN) is an adipokine concerned in the regulation of glucose metabolism, insulin sensitivity and fatty acid oxidation. APN plays a critical role in viral infections by regulating the immune response through its anti-inflammatory/pro-inflammatory axis. Reduction of APN may augment the severity of viral infections because APN inhibits immune cells’ response via suppression of inflammatory signaling pathways and stimulation of adenosine monophosphate protein kinase (AMPK). Moreover, APN inhibits the stimulation of nuclear factor kappa B (NF-κB) and regulates the release of pro-inflammatory cytokines, such as tumor necrosis factor alpha (TNF-α) and interleukins (IL-18, IL-6). In COVID-19, abnormalities of the fatty tissue due to oxidative stress (OS) and hyperinflammation may inhibit the production and release of APN. APN has lung-protective effect and can prevent SARS-CoV-2-induced acute lung injury (ALI) through the amelioration of endoplasmic reticulum (ER) stress, endothelial dysfunction (ED) and stimulation of peroxisome proliferator-activated receptor-alpha (PPAR-α). It has been established that there is a potential correlation between inflammatory signal transduction pathways and APN that contributes to the development of SARS-CoV-2 infections. Deregulation of these molecular pathways affects the expression of APN and vice versa. In addition, the reduction of APN effect in SARS-CoV-2 infection could be a potential cause of the exacerbation of pro-inflammatory effects which are associated with the disease severity. In this context, exploratory, developmental, and extensive prospective studies are necessary.