Figure 1.

Pathophysiology of complications associated with obesity in COVID-19. Obesity is a recognized risk factor for complications in SARS-Cov-2 infection, which is associated with various mechanisms. SARS-CoV-2 enters the cell through the interaction of the S protein with the ACE2 receptor expressed in various cell types. Proposed mechanisms include: (A) ACE2 expression in adipose tissue, which contributes to increased susceptibility to infection and viral systemic spread; (B) chronic inflammation and amplification of the pro-inflammatory response, characterized by a deregulation of the immune response associated with progression to severe and critical conditions characterized by multiple organ failure mediated by apoptosis and alteration of lung function, triggering different respiratory complications; and (C) endothelial damage and hypercoagulability, a phenomenon mediated by the direct cytotoxic action of the virus on the endothelial cell that expresses ACE2, generating endothelial disease and apoptosis. On the other hand, significant changes have been described in the expression of procoagulant proteins and regulation of fibrinolysis, release of microparticles derived from platelets and platelet activation induced by the generation of reactive oxygen species (ROS), which generates a state of hypercoagulability, predisposing the patient to the development of thrombosis.