作者: Akiyuki Nishimura , Caroline Sunggip , Sayaka Oda , Takuro Numaga-Tomita , Makoto Tsuda
DOI: 10.1016/J.PHARMTHERA.2017.06.010
关键词:
摘要: Purinergic signaling, mediated mainly by G protein-coupled P2Y receptors (P2YRs), is now attracting attention as a new therapeutic target for preventing or treating cardiovascular diseases. Observations using mice with genetically modified P2YRs and/or treated pharmacological P2YR inhibitor have helped us understand the physiological and pathological significance of in system. P2YR-mediated biological functions are predominantly activated mononucleotides released from non-adrenergic, non-cholinergic nerve endings non-secretory tissues response to physical stress cell injury, though recent studies suggested occurrence ligand-independent function through receptor-receptor interactions (oligomerization) several processes. In this review, we introduce possible dimerization (GPCRs) We focus especially on crosstalk between uridine nucleotide-responsive P2Y6R angiotensin (Ang) II type1 receptor (AT1R) our finding that antagonist MRS2578 interrupts heterodimerization AT1R, thereby reducing risk AT1R-stimulated hypertension mice. These results strongly suggest targeting oligomerization could be an effective strategy reduce