FIGURE 1.

Sex-biased mechanisms of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in the cardiovascular system. Following entry (I), SARS-CoV-2 is expected to be cadiotropic. However, the current view is that its myocardial localization is primarily due to infected immune cells invading the myocardial tissue (A). The host responds with systemic inflammation and cytokine storm (B), which contribute to cardiac and vascular injury (II). Dysregulation of angiotensin signaling, thromboinflammation and plasmin-associated hyperactive fibrinolysis-induced D-dimer increases (C) result in pronounced cell death and tissue injury, including microvascular dysfunction (II). Ultimately, these pathophysiological mechanisms modulated by sex lead to major cardiovascular complications (III) in a sex-dependent manner.