{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wen Y"],"funding":["NIDDK NIH HHS","NHLBI NIH HHS"],"pagination":["eade7287"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11405121"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(726)"],"pubmed_abstract":["Acute kidney injury (AKI) is a major risk factor for long-term adverse outcomes, including chronic kidney disease. In mouse models of AKI, maladaptive repair of the injured proximal tubule (PT) prevents complete tissue recovery. However, evidence for PT maladaptation and its etiological relationship with complications of AKI is lacking in humans. We performed single-nucleus RNA sequencing of 120,985 nuclei in kidneys from 17 participants with AKI and seven healthy controls from the Kidney Precision Medicine Project. Maladaptive PT cells, which exhibited transcriptomic features of dedifferentiation and enrichment in pro-inflammatory and profibrotic pathways, were present in participants with AKI of diverse etiologies. To develop plasma markers of PT maladaptation, we analyzed the plasma pro"],"journal":["Science translational medicine"],"pubmed_title":["Analysis of the human kidney transcriptome and plasma proteome identifies markers of proximal tubule maladaptation to injury."],"pmcid":["PMC11405121"],"funding_grant_id":["UH3 DK114866","U01 DK133090","U01 DK133081","U01 DK133092","U01 DK133091","U01 DK133093","U01 DK133095","U01 DK133097","UH3 DK114861","U01 DK114866","U01 DK114920","U01 DK133113","U01 DK114923","U01 DK114933","R01 HL085757","U01 DK133766","R01 DK093771","U01 DK133768","U01 DK114907","U24 DK114886","U01 DK114908","K01 DK120783"],"pubmed_authors":["Wen Y","Su E","Xu L","Mansour SG","Obeid W","Translational Investigation of Biomarker Endpoint of Acute Kidney Injury","Menez S","Cahan P","Devarajan P","Kidney Precision Medicine Project","Palevsky PM","Parikh CR","Cantley LG","Moledina DG"],"additional_accession":[]},"is_claimable":false,"name":"Analysis of the human kidney transcriptome and plasma proteome identifies markers of proximal tubule maladaptation to injury.","description":"Acute kidney injury (AKI) is a major risk factor for long-term adverse outcomes, including chronic kidney disease. In mouse models of AKI, maladaptive repair of the injured proximal tubule (PT) prevents complete tissue recovery. However, evidence for PT maladaptation and its etiological relationship with complications of AKI is lacking in humans. We performed single-nucleus RNA sequencing of 120,985 nuclei in kidneys from 17 participants with AKI and seven healthy controls from the Kidney Precision Medicine Project. Maladaptive PT cells, which exhibited transcriptomic features of dedifferentiation and enrichment in pro-inflammatory and profibrotic pathways, were present in participants with AKI of diverse etiologies. To develop plasma markers of PT maladaptation, we analyzed the plasma pro","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Dec","modification":"2026-07-15T05:36:00.305Z","creation":"2026-07-01T03:07:19.396Z"},"accession":"S-EPMC11405121","cross_references":{"pubmed":["38091407"],"doi":["10.1126/scitranslmed.ade7287"]}}