Mechanistic insight on the role of leukotriene receptors in ischemic-reperfusion injury.

Leukotrienes (LT) are a class of inflammatory mediators produced by the 5-lipoxygenase (5-LO) enzyme from arachidonic acid (AA). We discussed the various LT inhibitors and downstream pathway modulators, such as Mitogen-Activated Protein Kinases (MAPK), Phosphatidylinositol 3-Kinase/Protein Kinase B (PI3K/Akt), 5'-Adenosine Monophosphate-Activated Protein Kinase (AMPK), Protein Kinase C (PKC), Nitric Oxide (NO), Bradykinin, Early Growth Response-1 (Egr-1), Nuclear Factor-κB (NF-κB), and Tumor Necrosis Factor-Alpha (TNF-α), which in turn regulate various metabolic and physiological processes involving I/R injury. A systematic literature review of Bentham, Scopus, PubMed, Medline, and EMBASE (Elsevier) databases was carried out to understand the nature and mechanistic interventions of the leukotriene receptor modulations in ischemic injury. In the pathophysiology of I/R injuries, LT has been found to play an important role. I/R injury affects most of the vital organs and is characterized by inflammation, oxidative stress, cell death, and apoptosis leading to morbidity and mortality. sThis present review focuses on the various LT receptors, i.e., CysLT, LTC4, LTD4, and LTE4, involved in developing I/R injury in organs, such as the brain, spinal cord, heart, kidney, liver, and intestine.