Angiotensin-(1-7)-Mediated Signaling in Cardiomyocytes

Figure 4

Summary of current knowledge regarding Ang-(1-7) modulation of Ca²⁺ handling in ventricular myocytes and the underlying mechanisms. Acute treatment of cardiomyocytes with Ang-(1-7) apparently has no direct effect on Ca²⁺ handling (black circle, left). Lack of effect on Ca²⁺ levels was also observed in cardiomyocytes from TG rats with increased circulating levels of Ang-(1-7) (black circle, middle). In contrast, Ang-(1-7) signaling disruption through Mas genetic ablation (Mas KO) leads to Ca²⁺ dysfunction (red circle, right). Cardiomyocytes from Mas KO mice present reduced SERCA expression levels and Ca²⁺ transients (red arrows). Cardiac specific overexpression of Ang-(1-7) enhances Ca²⁺ release and SERCA levels in ventricular myocytes (green circle and arrows). Data regarding Ang-(1-7) modulation of some other key proteins involved in Ca²⁺ handling in ventricular myocytes, such as PLN, NCX, TnI, and TnC, are still missing. Black filled circles = calcium ions; LTCC = L-type Ca²⁺ channels; Mas = Mas receptor; NCX = Na⁺/Ca²⁺ exchanger; PLB = phospholamban; RyR = ryanodine receptor; TnC = troponin C; TnI = troponin I.