Fig. 1From: Direct mechanisms of SARS-CoV-2-induced cardiomyocyte damage: an updateMechanisms of direct myocardial injury induced by SARS-CoV-2. SARS-CoV-2 can enter into CMs through an endosomal-dependent mechanism. Cleaving the S protein into the S1 and S2 subunits exposes the RBD of the S1 subunit, allowing the virus to recognize and bind to the ACE2 receptor. SARS-CoV-2 invasion may cause direct myocardial injury through three mechanisms. (1) Nsp3 and Nsp5 production lead to the decrease of thin filaments and rupture of thick filaments, respectively. In addition, SARS-CoV-2 infection impairs the contractile function of CMs by altering gene expression profiles and reducing the mitochondrial oxidative phosphorylation levels. (2) The S protein promotes the formation of junctions between adjacent CMs and causes electrophysiological abnormalities. (3) Endocytosis and cleavage of ACE2 result in high AngII and low Ang (1–7) levels, leading to a decrease in anti-inflammatory processes and cardiomyocyte injury. CMs: cardiomyocytes; ACE2: angiotensin-converting enzyme 2; RBD: receptor-binding domain; Nsp: non-structure protein; ATP: adenosine triphosphate; Ang: angiotensin; ADAM17: A disintegrin and Metalloproteinase-17; AT1R: angiotensin II type-1 receptorBack to article page