Cardiomyocyte-derived small extracellular vesicles can signal eNOS activation in cardiac microvascular endothelial cells to protect against Ischemia/Reperfusion injury
Guihao Chen, Chuansheng Xu, Thomas G. Gillette, Tongyi Huang, Peisen Huang, Qing Li, Xiangdong Li, Qinfeng Li, Ning Yu, Ruijie Tang, Cunrong Huang, Yuyan Xiong, Xiaqiu Tian, Jun Xu, Junyan Xu, Liping Chang, Cong Wei, Chen Jin, Joseph A. Hill, Yuejin Yang
Abstract
These data uncover a mechanism by which the crosstalk between CMs and CMECs leads to the increased survival of the heart after I/R injury and point to a new therapeutic target for the blunting of myocardial I/R injury.
Topics & Concepts
EnosCardioprotectionReperfusion injuryIschemiaCrosstalkPharmacologyNitric oxideEndotheliumNitric oxide synthaseBiologyCell biologyMedicineCardiologyInternal medicineOpticsPhysicsLipid metabolism and disordersCancer-related molecular mechanisms researchATP Synthase and ATPases Research