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Update on the role and mechanism of erythropoietin receptor in acute kidney injury and repair or fibrosis

HAN Cheng1, LIU Yu1, WU Yuan-Yuan2, YANG Bin1,3,*

1Nantong-Leicester Joint Institute of Kidney Science, Department of Nephrology, Affiliated Hospital of Nantong University, Nantong 226001, China;2Department of Pathology, Medical School, Nantong University, Nantong 226001, China;3Renal Research Group, Cardiovascular Sciences, University of Leicester, University Hospitals of Leicester, Leicester, LE1 9HN, UK


Acute kidney injury (AKI) is a common critical disease clinically with high morbility and mortality and some survival patients also progress to chronic kidney disease. Renal ischemia-reperfusion (IR) is one of the main causes of AKI, in which, its repair and potential fibrosis, apoptosis, inflammation and phagocytosis play important roles. During the progression of IR-induced AKI, the expression of erythropoietin homodimer receptor (EPOR)2 and EPOR and β common receptor formed heterodimer receptor (EPOR/βcR) is changed dynamically. Moreover, (EPOR)2 and EPOR/βcR may synergistically participate in renoprotection at the stage of AKI and early repair, whereas at the late stage of AKI, the (EPOR)2 induces renal fibrosis and the EPOR/βcR facilitates repair and remodelling. The underlying mechanism, signaling pathways and the different effect turning point of (EPOR)2 and EPOR/βcR have not been well defined. It has been reported that EPO, according to its 3D structure, derived helix B surface peptide (HBSP) and cyclic HBSP (CHBP) only bind to EPOR/βcR. Synthesized HBSP, therefore, provides an effective tool to distinguish the different roles and mechanisms of both receptors, with the (EPOR)2 promoting fibrosis or the EPOR/βcR leading to repair/remodelling at the late stage of AKI. This review discusses the similarities and differences of (EPOR)2 and EPOR/βcR in their impacts on apoptosis, inflammation and phagocytosis in AKI, repair and fibrosis post IR, associated mechanisms, signaling pathways and outcomes. 

Key words: acute kidney injury; ischemia-reperfusion injury; erythropoietin receptor; repair; fibrosis

Received:   Accepted:

Corresponding author: YANG Bin  E-mail: ,

DOI: 10.13294/j.aps.2023.0002

Citing This Article:

HAN Cheng, LIU Yu, WU Yuan-Yuan, YANG Bin. Update on the role and mechanism of erythropoietin receptor in acute kidney injury and repair or fibrosis. Acta Physiol Sin 2023; 75 (1): 115-129 (in Chinese with English abstract).