Following acute cardiac injury such as myocardial infarction (MI), the controlled activation and recruitment of various leukocytes to the site of tissue damage significantly impacts chronic changes to cardiac structure and function, and ultimately host survival. While recent research has focused primarily on how leukocytes respond to injury, understanding how to effectively modulate their responsiveness to dampen maladaptive inflammation and promote repair processes is not yet fully understood. The complex spatio-temporal migration and activation of leukocytes are largely controlled by various chemokines and their cognate receptors, belonging to the G protein-coupled receptor (GPCR) family. Beyond chemokine receptors, leukocytes express a host of additional GPCRs that have recently been shown to regulate their responsiveness to cardiac injury. In this minireview, we will briefly discuss the impact of chemokine receptors on leukocyte behaviour, with subsequent focus on the most recent advancements in understanding the impact and therapeutic potential of other GPCR classes on leukocyte responses after acute cardiac injury.
Keywords: Adenosine; Cytokines; GPCR; Leukocytes; Leukotriene; Myocardial Infarction; Orphan Receptors; Prostaglandin; βAR.