PMC:7534795 / 13422-15208 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7534795","sourcedb":"PMC","sourceid":"7534795","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7534795","text":"Potential mechanisms of SARS-CoV-2-induced cardiovascular complications. SARS-Cov-2 may be taken up by cardiac cells using different routes, such as via ACE2 receptors expressed on the cell surface. Following entry, SARS-CoV-2 may exert cardiac injury by direct action and/or induction of immune responses resulting in release of pro-inflammatory cytokines (‘Cytokine storm’) such as IL, TNF-α, INF-γ, FGF, MCP1 and VEGF. SARS-CoV-2 can trigger the innate immune response involving NLRP3 inflammasomes which lead to activation of pro-inflammatory cytokines, IL-1β and IL-18 and the inflammatory cascade (IL-6 and TNF-α) resulting in tissue damage and fibrosis. SARS-CoV-2-induced pneumonia results in the development of hypoxemia which can impair Ca2+ homeostasis, increase ROS production and activate NLRP3 inflammasomes leading to cardiac damage. Activation of the sympathetic nervous system in response to pneumonia leads to vasoconstriction and tachycardia compromising coronary perfusion. This results in a mismatch of myocardial O2 demand and supply precipitating ischemia. SARS-CoV-2 can destabilize coronary atherosclerotic plaques and mediate platelet aggregation resulting in arterial and venous thrombosis. Altogether, these SARS-CoV-2 mediated effects may be contributing to the observed cardiovascular injury. ACE2, Angiotensin-converting enzyme-2; Ca2+, Calcium; FGF, Fibroblast growth factor; IL, Interleukin; INF, Interferon; MCP-1, Monocyte chemoattractant protein-1; NFκB, Nuclear factor kappa-light-chain enhancer activated B-cells; NLRP3, NACHT, LRR and PYD domains-containing protein 3; O2, Oxygen; ROS, Reactive oxygen species; SARS-CoV-2, Severe and acute respiratory syndrome coronavirus; TNF-α, Tumor necrosis factor-α; VEGF, Vascular endothelial growth 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