Update on the role and mechanism of erythropoietin receptor in acute kidney injury and repair or fibrosis.
- Author:
Cheng HAN
1
;
Yu LIU
1
;
Yuan-Yuan WU
2
;
Bin YANG
1
Author Information
1. Nantong-Leicester Joint Institute of Kidney Science, Department of Nephrology, Affiliated Hospital of Nantong University, Nantong 226001, China.
2. Department of Pathology, Medical School, Nantong University, Nantong 226001, China. see-andy@163.com.
- Publication Type:Journal Article
- MeSH:
Humans;
Receptors, Erythropoietin;
Acute Kidney Injury;
Apoptosis;
Inflammation;
Phagocytosis;
Reperfusion Injury
- From:
Acta Physiologica Sinica
2023;75(1):115-129
- CountryChina
- Language:Chinese
-
Abstract:
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.
