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Ang II and ET-1, via G-protein-coupled receptors, activate growth factor receptors including IGF-1, PDGF, and EGF, thereby increasing redox-dependent vascular processes such as vascular remodeling, inflammation, medial hypertrophy, and fibrosis (63)

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With studies characterising reduced infarct size, improved cardiac function, promotion of cardiac progenitor cell migration, cardiomyocyte survival through PI3K/Akt anti-apoptotic signalling, and stimulation of new vessel formation in infarcted myocardium

It can be hijacked to promote tumorigenesis via stress adaptation, metabolic reprogramming and immune evasion

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