Protective effects of endogenous and exogenous Annexin A1 on ischemia-reperfusion-derived injuries

Abstract

Ischemia and reperfusion (I/R) injury permeates a variety of diseases, causing significant inflammatory and thrombotic responses. Given its importance, efforts have been made to identify the complex and integrated network of mediators that ensure a timely and spatially regulated inflammatory response, in order to mitigate its deleterious effects on the body. The Annexin A1 protein (ANXA1) and its mimetic peptide Ac2-26 can alleviate the inflammatory process by decreasing adhesion and neutrophil trafficking, inhibiting pro-inflammatory and pro-thrombotic mediators, and regulating the interactions of neutrophil-platelets. In this review, we discuss the anti-inflammatory potential of ANXA1 and its intracellular effects, contrasting the possible long-term permanence of the damage caused by I/R injuries. As a pharmacological approach, the aim is to understand how ANXA1 operates in processes resulting from I/R injuries and its performance as a biomarker and therapeutic target after injury in different tissues and organs.