Verma Sudhanshu Kumar, Molitoris Bruce A
Nephrology Division, Department of Medicine, Indiana University School of Medicine, The Roudebush VA Medical Center, Indiana Center for Biological Microscopy, Indianapolis, IN.
Nephrology Division, Department of Medicine, Indiana University School of Medicine, The Roudebush VA Medical Center, Indiana Center for Biological Microscopy, Indianapolis, IN.
Semin Nephrol. 2015 Jan;35(1):96-107. doi: 10.1016/j.semnephrol.2015.01.010.
The kidney is comprised of heterogeneous cell populations that function together to perform a number of tightly controlled, complex and interdependent processes. Renal endothelial cells contribute to vascular tone, regulation of blood flow to local tissue beds, modulation of coagulation and inflammation, and vascular permeability. Both ischemia and sepsis have profound effects on the renal endothelium, resulting in microvascular dysregulation resulting in continued ischemia and further injury. In recent years, the concept of the vascular endothelium as an organ that is both the source of and target for inflammatory injury has become widely appreciated. Here we revisit the renal endothelium in the light of ever evolving molecular advances.
肾脏由异质性细胞群组成，这些细胞群共同发挥作用，执行许多严格控制、复杂且相互依存的过程。肾内皮细胞有助于调节血管张力、控制局部组织床的血流、调节凝血和炎症反应以及维持血管通透性。缺血和脓毒症均会对肾内皮产生深远影响，导致微血管调节功能紊乱，进而持续缺血并造成进一步损伤。近年来，血管内皮作为炎症损伤的源头和靶点这一器官的概念已得到广泛认可。在此，我们根据不断发展的分子学进展重新审视肾内皮。
