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
Corresponding author: YANG Bin E-mail: ,
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).