The present study reveals that both ACE and ACE2 bind integrins in an RGD-independent manner. We have shown that ACE2, in particular, increases cellular adhesion and, moreover, affects integrin signalling. Shedding of the ACE2 protein may relieve repression of integrin signalling, exerted by the presence of ACE2 on the cell membrane. Using primary cardiac myofibroblasts we have demonstrated that the actions of ACE and ACE2 exerted on cell models are physiologically relevant to the diseased human heart.