Role of Purinergic Signalling in Endothelial Dysfunction and Thrombo-Inflammation in Ischaemic Stroke and Cerebral Small Vessel Disease

The cerebral endothelium is an active interface between blood and the central nervous system. In addition to being a physical barrier brain, also actively regulates metabolic homeostasis, vascular tone permeability, coagulation, movement of immune cells. Being part blood–brain barrier, endothelial cells brain have specialized morphology, physiology, phenotypes due their unique microenvironment. Known cardiovascular risk factors facilitate dysfunction, leading impaired vasodilation, aggravated inflammatory response, as well increased oxidative stress proliferation. This culminates in thrombo-inflammatory underlying cause ischemic stroke small vessel disease (CSVD). These events are further exacerbated when flow returned after period ischemia, phenomenon termed ischemia-reperfusion injury. Purinergic signaling endogenous molecular pathway which enzymes CD39 CD73 catabolize extracellular adenosine triphosphate (eATP) adenosine. After ischemia CSVD, eATP released from dying neurons damage molecule, triggering thrombosis inflammation. contrast, anti-thrombotic, protects against stress, suppresses response. Evidently, therapies that promote generation or boost activity at site injury promising benefits context atherothrombotic can be extended current CSVD known pathomechanisms. Here, we reviewed rationale treat dysfunction brain.