AGT and systemic sclerosis: The pathophysiological mechanisms of SSc, like detrimental vasoconstriction, pro-inflammatory, proliferative, and pro-fibrotic effects, are mediated by angiotensin II (Ang II) and endothelin 1 (ET1) through type I angiotensin II receptor (AT1R) and endothelin I receptor (ETAR), respectively [51].