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Immune Cells in Ischemic Acute Kidney Injury

[ Vol. 20 , Issue. 8 ]

Author(s):

Long Zheng, Wenjun Gao, Chao Hu, Cheng Yang* and Ruiming Rong*   Pages 770 - 776 ( 7 )

Abstract:


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.

Keywords:

Ischemic, acute kidney injury, immune cells, renal function, chemokines, cytokines.

Affiliation:

Shanghai Key laboratory of Organ Transplantation, 180 Fenglin Road, Shanghai 200032, Shanghai Key laboratory of Organ Transplantation, 180 Fenglin Road, Shanghai 200032, Shanghai Key laboratory of Organ Transplantation, 180 Fenglin Road, Shanghai 200032, Shanghai Key laboratory of Organ Transplantation, 180 Fenglin Road, Shanghai 200032, Department of Urology, Zhongshan Hospital, Fudan University, Shanghai 200032

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