急性肾损伤
免疫系统
发病机制
趋化因子
医学
肾
免疫学
炎症
缺血
肾缺血
先天免疫系统
再灌注损伤
内科学
作者
Long Zheng,Wen‐Jun Gao,Chao Hu,Cheng Yang,Ruiming Rong
出处
期刊:Current Protein & Peptide Science
[Bentham Science]
日期:2019-05-07
卷期号:20 (8): 770-776
被引量:33
标识
DOI:10.2174/1389203720666190507102529
摘要
Acute kidney injury (AKI) is a systemic disease characterized by acute loss of renal function and accumulation of end products of nitrogen metabolism. Ischemic AKI is the most common cause of AKI, and inflammatory responses are inevitablely involved in ischemic AKI. In the process of ischemic AKI, multiple factors are involved in activating and recruitment of immune cell to the injured kidney. These factors include DAMPs and HIFs released from the injured kidney, increased expression of adhesion molecules, the production of chemokines and cytokines, activation of complement system and TLRs as well as the permeability dysfunction of the renal vascular endothelium. Immune cells of both the innate and adaptive immune systems, such as neutrophils, dendritic cells, macrophages and lymphocytes contribute to the pathogenesis of renal injury after ischemia reperfusion injury (IRI), with some of their subpopulations also participating in the repair process. Numerous studies of immune cells involved in the pathogenesis of AKI have enhanced the understanding of their possible mechanisms in AKI which might become the potential targets for the treatment of ischemic AKI. This review describes the function of the immune cells in the pathogenesis and repair of ischemic AKI and emphasizes the treatment of ischemic AKI potentially targeting them.
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