{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang J"],"funding":["National Natural Science Foundation of China","National Natural Science Foundation of China (National Science Foundation of China)"],"pagination":["44"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7925512"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["7(1)"],"pubmed_abstract":["Ischemia-reperfusion (IR) injury to the renal epithelia is associated with endoplasmic reticulum stress (ERS) and mitochondria dysfunction, which lead to oxidative stress-induced acute kidney injury (AKI). X-box binding protein 1 (XBP1), an ERS response protein, could play a prominent role in IR-induced AKI. In this study, we revealed that XBP1 and its downstream target HRD1 participated in the crosstalk between ERS and mitochondrial dysfunction via regulation of NRF2/HO-1-mediated reactive oxidative stress (ROS) signaling. Mice with reduced expression of XBP1 (heterozygous Xbp1±) were resistant to IR-induced AKI due to the enhanced expression of NRF2/HO-1 and diminished ROS in the kidney. Downregulation of XBP1 in renal epithelial cells resulted in reduced HRD1 expression and increased NR"],"journal":["Cell death discovery"],"pubmed_title":["Downregulation of XBP1 protects kidney against ischemia-reperfusion injury via suppressing HRD1-mediated NRF2 ubiquitylation."],"pmcid":["PMC7925512"],"funding_grant_id":["81570678","81500573","81873623"],"pubmed_authors":["Wang M","Zhang J","Ni H","Chen G","Gong N","Miao Y","Katwal G","Li Q","Wang Y","Zhao Y","Sun K"],"additional_accession":[]},"is_claimable":false,"name":"Downregulation of XBP1 protects kidney against ischemia-reperfusion injury via suppressing HRD1-mediated NRF2 ubiquitylation.","description":"Ischemia-reperfusion (IR) injury to the renal epithelia is associated with endoplasmic reticulum stress (ERS) and mitochondria dysfunction, which lead to oxidative stress-induced acute kidney injury (AKI). X-box binding protein 1 (XBP1), an ERS response protein, could play a prominent role in IR-induced AKI. In this study, we revealed that XBP1 and its downstream target HRD1 participated in the crosstalk between ERS and mitochondrial dysfunction via regulation of NRF2/HO-1-mediated reactive oxidative stress (ROS) signaling. Mice with reduced expression of XBP1 (heterozygous Xbp1±) were resistant to IR-induced AKI due to the enhanced expression of NRF2/HO-1 and diminished ROS in the kidney. Downregulation of XBP1 in renal epithelial cells resulted in reduced HRD1 expression and increased NR","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Mar","modification":"2026-07-14T14:39:24.394Z","creation":"2025-04-21T17:06:57.041Z"},"accession":"S-EPMC7925512","cross_references":{"pubmed":["33654072"],"doi":["10.1038/s41420-021-00425-z"]}}