Endothelial cells: potential novel regulators of renal inflammation.
Endothelial cells: potential novel regulators of renal inflammation.
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内皮细胞：肾脏炎症的潜在新型调节剂。
DOI：
10.1152/ajprenal.00371.2021
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发表时间：
2022
期刊：
影响因子：
--
通讯作者：
VanBeusecum,JustinP
中科院分区：
文献类型：
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作者：
Oates,JimC;Russell,DayviaL;VanBeusecum,JustinP
大量证据支持内皮细胞（EC）活化和功能障碍在高血压、慢性肾脏病（CKD）和狼疮性肾炎（LN）发展中的作用。在人类和高血压、CKD和LN的实验模型中，EC被激活并释放有效的炎症介质，包括引起EC功能障碍、组织损伤和纤维化的细胞因子、趋化因子和活性氧。激活内皮的因素包括炎性细胞因子、机械拉伸和病理性剪切应力。这些信号可以激活内皮以促进粘附分子的上调，例如细胞间粘附分子-1和血管细胞粘附分子-1，其促进白细胞粘附和迁移到激活的内皮。更重要的是，现在认识到，这些信号中的一些可能反过来促进内皮抗原呈递通过主要组织相容性复合物II。在这篇综述中，我们将考虑深入的机制，内皮细胞活化和新的机制，内皮抗原呈递。此外，我们还将讨论肾脏病理中的这些促炎事件，并考虑可能的新治疗方法，以限制高血压、CKD和LN中内皮炎症的不良影响。
Substantial evidence has supported the role of endothelial cell (EC) activation and dysfunction in the development of hypertension, chronic kidney disease (CKD), and lupus nephritis (LN). In both humans and experimental models of hypertension, CKD, and LN, ECs become activated and release potent mediators of inflammation including cytokines, chemokines, and reactive oxygen species that cause EC dysfunction, tissue damage, and fibrosis. Factors that activate the endothelium include inflammatory cytokines, mechanical stretch, and pathological shear stress. These signals can activate the endothelium to promote upregulation of adhesion molecules, such as intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, which promote leukocyte adhesion and migration to the activated endothelium. More importantly, it is now recognized that some of these signals may in turn promote endothelial antigen presentation through major histocompatibility complex II. In this review, we will consider in-depth mechanisms of endothelial activation and the novel mechanism of endothelial antigen presentation. Moreover, we will discuss these proinflammatory events in renal pathologies and consider possible new therapeutic approaches to limit the untoward effects of endothelial inflammation in hypertension, CKD, and LN.