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O-Glycosylation of E-Cadherin Induced by Endoplasmic Reticulum Stress Negatively Regulates Cell Polarity and Proliferation in Acute Kidney Injury
1 Introduction Acute kidney injury (AKI), a clinical syndrome characterized by a sudden decline in renal function within several hours or days [1-3], greatly contributes to the development and progression of chronic kidney diseases (CKD) and end-stage renal diseases (ESRD) [4]. Currently, most management strategies for AKI are supportive, lacking effective methods to mitigate kidney injury and promote the recovery of renal function [5].
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