{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lin Q"],"funding":["Public health Industry Project of Shanghai Municipal Health commission","Shanghai Municipal Commission of Health and Family Planning, and Office for Traditional Chinese Medicine Development of Shanghai","Outstanding Youth Project from Shanghai key laboratory of nucleic acid chemistry and nanomedicine","National Natural Science Foundation of China","Shanghai Municipal Health Commission and Family Planning","Shanghai Sailing Program"],"pagination":["2975-2990"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8525960"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["17(10)"],"pubmed_abstract":["The pathogenetic mechanism of contrast-induced acute kidney injury (CI-AKI), which is the third most common cause of hospital-acquired AKI, has not been elucidated. Previously, we demonstrated that renal injury and cell apoptosis were attenuated in <i>nlrp3</i> knockout CI-AKI mice. Here, we investigated the mechanism underlying NLRP3 inhibition-mediated attenuation of apoptosis in CI-AKI. The RNA sequencing analysis of renal cortex revealed that the <i>nlrp3</i> or <i>casp1</i> knockout CI-AKI mice exhibited upregulated cellular response to hypoxia, mitochondrial oxidation, and autophagy when compared with the wild-type (WT) CI-AKI mice, which indicated that NLRP3 inflammasome inhibition resulted in the upregulation of hypoxia signaling pathway and mitophagy. The <i>nlrp3</i> or <i>casp1<"],"journal":["Autophagy"],"pubmed_title":["Inhibiting NLRP3 inflammasome attenuates apoptosis in contrast-induced acute kidney injury through the upregulation of HIF1A and BNIP3-mediated mitophagy."],"pmcid":["PMC8525960"],"funding_grant_id":["81770666","81570604","81370794","2020ZYA002","20YF1424900","81700586","20194Y0332","ZY (2018–2020)-FWTX-1001","ZHYY-ZXYJHZX-1-02"],"pubmed_authors":["Wu J","Lin Q","Shen J","Zhang M","Zhou W","Jiang N","Ni Z","Shao X","Jin H","Li S","Zhang Z","Gu L","Zhu X","Lu R"],"additional_accession":[]},"is_claimable":false,"name":"Inhibiting NLRP3 inflammasome attenuates apoptosis in contrast-induced acute kidney injury through the upregulation of HIF1A and BNIP3-mediated mitophagy.","description":"The pathogenetic mechanism of contrast-induced acute kidney injury (CI-AKI), which is the third most common cause of hospital-acquired AKI, has not been elucidated. Previously, we demonstrated that renal injury and cell apoptosis were attenuated in <i>nlrp3</i> knockout CI-AKI mice. Here, we investigated the mechanism underlying NLRP3 inhibition-mediated attenuation of apoptosis in CI-AKI. The RNA sequencing analysis of renal cortex revealed that the <i>nlrp3</i> or <i>casp1</i> knockout CI-AKI mice exhibited upregulated cellular response to hypoxia, mitochondrial oxidation, and autophagy when compared with the wild-type (WT) CI-AKI mice, which indicated that NLRP3 inflammasome inhibition resulted in the upregulation of hypoxia signaling pathway and mitophagy. The <i>nlrp3</i> or <i>casp1<","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Oct","modification":"2025-04-22T11:26:45.047Z","creation":"2025-04-06T00:01:00.439Z"},"accession":"S-EPMC8525960","cross_references":{"pubmed":["33345685"],"doi":["10.1080/15548627.2020.1848971"]}}