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nature portfolio privacy policy pbobi-n-gfp-mgpx4 vectors fsp1fl/flkspcre-ert2 mice showed induced gpx4fl/flkspcre-ert2 mice advertising acsl4fl/flkspcre-ert2 mice revealed nature gpx4fl/flkspcre-ert2 mice subjected middle-aged leaders social media fsp1fl/flkspcre-ert2 mice specific pathogen-free conditions caox-induced cell death reprints acsl4fl/flkspcre-ert2 mice fsp1fl/flkspcre-ert2 groups full size image pbobi-c-gfp-mfsp1 acsl4wt/wtkspcre-ert2 mice crystal-induced kidney injury fujian research oxalate-induced kidney injury acsl4fl/flkspcre-ert2 groups n-terminal gfp tag fsp1fl/flkspcre cko mice renal tubule-specific deletion renal tubule-specific deficiency aggravated oxalate-induced aki crossing fsp1fl/fl mice copper-dependent autophagic degradation fsp1wt/wtkspcre-ert2 mice acsl4wt/wtkspcre-ert2 groups ferroptosis-specific inhibitor ferrostatin-1 previous research lactis mg1363-pmg36e-glp-1 reduced pi-positive ratio induce oxalate-induced aki crossing acsl4fl/fl mice acute kidney injury oxalate-induced aki mice oxalate-induced aki model ischemia-reperfusion injury kspcre-ert2 transgenic mice fsp1wt/wtkspcre-ert2 groups tail-snip polymerase pcr acyl-coa synthase acsl4 stable gpx4-deficient ptecs ox-c11 cell ratios free access

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         description:Ferroptosis has emerged as a crucial driver of injury in various organs, including acute kidney injury (AKI). However, the regulatory roles and underlying mechanisms of key genes involved in ferroptosis during oxalate-induced AKI are not fully understood. In this study, we conducted single-cell RNA sequencing (scRNA-seq) analysis of kidney samples, revealing the occurrence of ferroptosis in renal tubular cells of an oxalate-induced AKI mouse model, which was confirmed in subsequent in vitro experiments. Furthermore, renal tubule-specific deficiency of Acsl4 conferred significant protection against oxalate-induced AKI, as evidenced by alleviated structural and functional renal damage, reduced oxidative stress and decreased inflammatory cell infiltration, all of which collectively contribute to a reduction in ferroptosis. In contrast, Fsp1 deficiency exacerbated these pathological processes. Consistent with the in vivo findings, Acsl4 knockout in mouse renal tubular epithelial cell lines (MTECs) resulted in decreased lipid peroxidation and mitigation of mitochondrial dysfunction, thus reducing calcium oxalate (CaOX)-induced ferroptosis. Conversely, Fsp1 knockout in MTECs had the opposite effects. In addition, as expected, overexpression of the ferroptosis inhibitors GPX4 or FSP1 in MTECs significantly reduced CaOX-induced lipid peroxidation and cell ferroptosis. In summary, these findings indicated that oxalate exposure upregulated ferroptosis driver ACSL4 and downregulated inhibitors like GPX4 and FSP1, leading to lipid peroxidation and mitochondrial dysfunction, which collectively triggered ferroptosis in renal tubular cells. Modulating ACSL4/GPX4 and FSP1 axes presents a promising therapeutic strategy for oxalate-induced AKI.
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      description:Ferroptosis has emerged as a crucial driver of injury in various organs, including acute kidney injury (AKI). However, the regulatory roles and underlying mechanisms of key genes involved in ferroptosis during oxalate-induced AKI are not fully understood. In this study, we conducted single-cell RNA sequencing (scRNA-seq) analysis of kidney samples, revealing the occurrence of ferroptosis in renal tubular cells of an oxalate-induced AKI mouse model, which was confirmed in subsequent in vitro experiments. Furthermore, renal tubule-specific deficiency of Acsl4 conferred significant protection against oxalate-induced AKI, as evidenced by alleviated structural and functional renal damage, reduced oxidative stress and decreased inflammatory cell infiltration, all of which collectively contribute to a reduction in ferroptosis. In contrast, Fsp1 deficiency exacerbated these pathological processes. Consistent with the in vivo findings, Acsl4 knockout in mouse renal tubular epithelial cell lines (MTECs) resulted in decreased lipid peroxidation and mitigation of mitochondrial dysfunction, thus reducing calcium oxalate (CaOX)-induced ferroptosis. Conversely, Fsp1 knockout in MTECs had the opposite effects. In addition, as expected, overexpression of the ferroptosis inhibitors GPX4 or FSP1 in MTECs significantly reduced CaOX-induced lipid peroxidation and cell ferroptosis. In summary, these findings indicated that oxalate exposure upregulated ferroptosis driver ACSL4 and downregulated inhibitors like GPX4 and FSP1, leading to lipid peroxidation and mitochondrial dysfunction, which collectively triggered ferroptosis in renal tubular cells. Modulating ACSL4/GPX4 and FSP1 axes presents a promising therapeutic strategy for oxalate-induced AKI.
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            name:Fujian Medical University
            address:
               name:Department of Nephrology, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
               type:PostalAddress
            type:Organization
      name:Kunmei Lai
      affiliation:
            name:Fujian Medical University
            address:
               name:Department of Nephrology, Blood Purification Research Center, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
               type:PostalAddress
            type:Organization
            name:Fujian Medical University
            address:
               name:Research Center for Metabolic Chronic Kidney Disease, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
               type:PostalAddress
            type:Organization
            name:Fujian Medical University
            address:
               name:Department of Nephrology, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
               type:PostalAddress
            type:Organization
      name:Yankun Song
      affiliation:
            name:Fujian Medical University
            address:
               name:Department of Pathology, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
               type:PostalAddress
            type:Organization
      name:Guoping Li
      affiliation:
            name:Fujian Medical University
            address:
               name:Department of Pathology, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
               type:PostalAddress
            type:Organization
      name:Huabin Ma
      affiliation:
            name:Fujian Medical University
            address:
               name:Central Laboratory, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
               type:PostalAddress
            type:Organization
      name:Hong Chen
      affiliation:
            name:Fujian Medical University
            address:
               name:Department of Pathology, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
               type:PostalAddress
            type:Organization
      name:Yanfang Xu
      url:http://orcid.org/0000-0002-6207-545X
      affiliation:
            name:Fujian Medical University
            address:
               name:Department of Nephrology, Blood Purification Research Center, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
               type:PostalAddress
            type:Organization
            name:Fujian Medical University
            address:
               name:Research Center for Metabolic Chronic Kidney Disease, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
               type:PostalAddress
            type:Organization
            name:Fujian Medical University
            address:
               name:Department of Nephrology, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
               type:PostalAddress
            type:Organization
            name:Fujian Medical University
            address:
               name:Central Laboratory, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Nephrology, Blood Purification Research Center, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
      name:Research Center for Metabolic Chronic Kidney Disease, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
      name:Department of Nephrology, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
      name:Central Laboratory, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
      name:Department of Nephrology, Blood Purification Research Center, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
      name:Research Center for Metabolic Chronic Kidney Disease, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
      name:Department of Nephrology, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
      name:Department of Nephrology, Blood Purification Research Center, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
      name:Research Center for Metabolic Chronic Kidney Disease, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
      name:Department of Nephrology, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
      name:Department of Pathology, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
      name:Department of Pathology, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
      name:Central Laboratory, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
      name:Department of Pathology, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
      name:Department of Nephrology, Blood Purification Research Center, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
      name:Research Center for Metabolic Chronic Kidney Disease, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
      name:Department of Nephrology, National Regional Medical Center, Binhai Campus of the First Affiliated Hospital, Fujian Medical University, Fuzhou, China
      name:Central Laboratory, the First Affiliated Hospital, Fujian Medical University, Fuzhou, China

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