The Renin-Angiotensin-Aldosterone System as a Therapeutic Target in Late Injury Caused by Ischemia-Reperfusion

Table 1

Therapeutic targets in the RAAS modulation.

Family	Molecular mechanism	Cell signaling modulation	Proposal therapeutic indication
AT1 inhibitors	Direct and selective blockage of the receptor	Survival, apoptosis, autophagy, TME, and fibrosis	After the first 72 h
ACE inhibitors	Blockage of the activity of the ACE	Apoptosis, proliferation, and fibrosis	In the late phase of I/R injury 7–14 days after injury
Renin inhibitors	Direct inhibition	Apoptosis, proliferation, and fibrosis	In the first hours of the injury
Mineralocorticoid receptor antagonists	Direct blockage of the receptor	Survival, apoptosis, autophagy, TME, and fibrosis	In the first hours of the injury
Aldosterone synthase inhibitors	Inhibition in the activity of the enzyme	Survival, apoptosis, autophagy, TME, and fibrosis	In the first hours of the injury
Modulation in the redox signaling and oxidative stress	Oxidative scavengers	Survival, apoptosis, autophagy, TME, and fibrosis	Before the injury and during the whole I/R phenomenon