{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Xie L"],"funding":["Shandong Provincial Natural Science Foundation","Qingdao Science and Technology Benefit People Demonstration Guide Special Project","National Natural Science Foundation of China","Shandong Province Major Scientific and Technical Innovation Project"],"pagination":["120"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12372359"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(1)"],"pubmed_abstract":["<h4>Background</h4>Spinal cord ischemia reperfusion injury (SCIRI) is a serious disease that can result in irreversible neuronal damage, leading to the loss of sensory and motor function. Cuproptosis, a novel form of regulated cell death, has been studied in various diseases. However, the role and mechanism of cuproptosis in SCIRI remain to be elucidated.<h4>Results</h4>The results of transcriptome analysis showed significant downregulation of ATP7B, which regulates copper ion efflux. Concurrently, another key cuproptosis-related gene, FDX1, was significantly altered. Thus, we performed qPCR and Western blot assays in vivo and in vitro to detect changes in cuproptosis-related genes. The results indicated that cuproptosis was indeed activated by SCIRI or OGD/R. Moreover, immunofluorescence/immunohistochemitry staining and neuronal activity tests were consistent with the above results. Furthermore, we also proved that ammonium tetrathiomolybdate, a copper chelator and cuproptosis inhibitor, could not only ameliorate neuronal damage and promote neuronal survival but also improve lower limb motor dysfunction.<h4>Conclusions</h4>SCIRI caused ATP7B downregulation, which blocked copper ion efflux, leading to copper ion accumulation, DLAT oligomerization, degradation of iron-sulfur cluster proteins and ultimately cuproptosis in neurons."],"journal":["Cell & bioscience"],"pubmed_title":["Spinal cord ischemia reperfusion injury induces cuproptosis in neurons."],"pmcid":["PMC12372359"],"funding_grant_id":["ZR2024QH590","22-3-7-smjk-5-nsh","82401552","2021SFGC0502","82472431"],"pubmed_authors":["Xiao X","Xie L","Shi W","Yu T","He Q","Wu H"],"additional_accession":[]},"is_claimable":false,"name":"Spinal cord ischemia reperfusion injury induces cuproptosis in neurons.","description":"<h4>Background</h4>Spinal cord ischemia reperfusion injury (SCIRI) is a serious disease that can result in irreversible neuronal damage, leading to the loss of sensory and motor function. Cuproptosis, a novel form of regulated cell death, has been studied in various diseases. However, the role and mechanism of cuproptosis in SCIRI remain to be elucidated.<h4>Results</h4>The results of transcriptome analysis showed significant downregulation of ATP7B, which regulates copper ion efflux. Concurrently, another key cuproptosis-related gene, FDX1, was significantly altered. Thus, we performed qPCR and Western blot assays in vivo and in vitro to detect changes in cuproptosis-related genes. The results indicated that cuproptosis was indeed activated by SCIRI or OGD/R. Moreover, immunofluorescence/immunohistochemitry staining and neuronal activity tests were consistent with the above results. Furthermore, we also proved that ammonium tetrathiomolybdate, a copper chelator and cuproptosis inhibitor, could not only ameliorate neuronal damage and promote neuronal survival but also improve lower limb motor dysfunction.<h4>Conclusions</h4>SCIRI caused ATP7B downregulation, which blocked copper ion efflux, leading to copper ion accumulation, DLAT oligomerization, degradation of iron-sulfur cluster proteins and ultimately cuproptosis in neurons.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Aug","modification":"2026-06-30T03:23:26.765Z","creation":"2026-06-30T03:16:15.846Z"},"accession":"S-EPMC12372359","cross_references":{"pubmed":["40841965"],"doi":["10.1186/s13578-025-01463-1"]}}