biostudies-literatureLin QPublic health Industry Project of Shanghai Municipal Health commissionShanghai Municipal Commission of Health and Family Planning, and Office for Traditional Chinese Medicine Development of ShanghaiOutstanding Youth Project from Shanghai key laboratory of nucleic acid chemistry and nanomedicineNational Natural Science Foundation of ChinaShanghai Municipal Health Commission and Family PlanningShanghai Sailing Program2975-2990https://www.ebi.ac.uk/biostudies/studies/S-EPMC8525960biostudies-literatureUnknown17(10)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<AutophagyInhibiting NLRP3 inflammasome attenuates apoptosis in contrast-induced acute kidney injury through the upregulation of HIF1A and BNIP3-mediated mitophagy.PMC85259608177066681570604813707942020ZYA00220YF14249008170058620194Y0332ZY (2018–2020)-FWTX-1001ZHYY-ZXYJHZX-1-02Wu JLin QShen JZhang MZhou WJiang NNi ZShao XJin HLi SZhang ZGu LZhu XLu RfalseInhibiting NLRP3 inflammasome attenuates apoptosis in contrast-induced acute kidney injury through the upregulation of HIF1A and BNIP3-mediated mitophagy.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<2021-01-01T00:00:00Z2021 Oct2025-04-22T11:26:45.047Z2025-04-06T00:01:00.439ZS-EPMC85259603334568510.1080/15548627.2020.1848971