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10.1007/s12033-025-01534-1 http://scihub22266oqcxt.onion/10.1007/s12033-025-01534-1 41353678!?!41353678 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=41353678&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Mol+Biotechnol 2025 ; ? (?): ? Nephropedia Template TP {{tp|p=41353678|t=2025. CMKLR1 as a Therapeutic Target: Vitamin D-Mediated Suppression of Inflammation and Oxidative Stress in SA-AKI |pdf=|usr=}}{{41353678}} gab.com Text CMKLR1 as a Therapeutic Target: Vitamin D-Mediated Suppression of Inflammation and Oxidative Stress in SA-AKI JO: Mol Biotechnol http://www.kidney.de/pget.php?&tw=1&pmid=41353678 #FOAvip Sepsis-associated acute kidney injury (SA-AKI) is a severe complication of sepsis, primarily driven by immune-inflammatory dysregulation and oxidative stress, and 1,25-Dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) shows renoprotective potential, yet its molecular targets and mechanisms remain unclear. Transcriptomic data of SA-AKI from GEO were analyzed by ssGSEA for immune infiltration, differential expression analysis, WGCNA, and machine learning (LASSO, SVM-RFE, Random Forest) to identify the biomarkers. In vivo, SA-AKI was induced by cecal ligation and puncture (CLP) in mice treated with 1,25(OH)(2)D(3,) and renal function, histology, inflammatory cytokines, oxidative stress markers, and CMKLR1 expression were evaluated. In vitro, LPS-stimulated HK-2 cells were treated with 1,25(OH)(2)D(3) with or without CMKLR1 overexpression to assess cytokines, cell viability, apoptosis, and oxidative stress. Four key biomarkers-CMKLR1, COL1A1, RPS19, and THBS1-were identified by machine learning, with CMKLR1 as the key target. In SA-AKI mice, 1,25(OH)(2)D(3) downregulated CMKLR1, improved renal function, and reduced inflammation and oxidative stress. In LPS-stimulated HK-2 cells, it dose-dependently suppressed cytokine release, restored cell viability, and alleviated oxidative stress, while CMKLR1 overexpression partially reversed these effects. CMKLR1 was identified as a key immune inflammation target in SA-AKI. 1,25(OH)(2)D(3) was protected against renal injury by suppressing CMKLR1, and mitigating inflammation, oxidative stress, and apoptosis, while CMKLR1 overexpression partially reversed these effects. These findings highlight CMKLR1 as a potential therapeutic target for SA-AKI. Twit Text FOAVip CMKLR1 as a Therapeutic Target: Vitamin D-Mediated Suppression of Inflammation and Oxidative Stress in SA-AKI ????Mol Biotechnol http://www.kidney.de/pget.php?&tw=1&pmid=41353678 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=41353678 #FOAvip English Wikipedia <ref>{{Cite pmid|41353678}}</ref> CMKLR1 as a Therapeutic Target: Vitamin D-Mediated Suppression of Inflammation and Oxidative Stress in SA-AKI #MMPMID41353678 Wang J; Guo R; Wang L; Guo J; Bayinchahan B; Wang Z; Xiao D Mol Biotechnol 2025[Dec]; ? (?): ? PMID41353678show ga Sepsis-associated acute kidney injury (SA-AKI) is a severe complication of sepsis, primarily driven by immune-inflammatory dysregulation and oxidative stress, and 1,25-Dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) shows renoprotective potential, yet its molecular targets and mechanisms remain unclear. Transcriptomic data of SA-AKI from GEO were analyzed by ssGSEA for immune infiltration, differential expression analysis, WGCNA, and machine learning (LASSO, SVM-RFE, Random Forest) to identify the biomarkers. In vivo, SA-AKI was induced by cecal ligation and puncture (CLP) in mice treated with 1,25(OH)(2)D(3,) and renal function, histology, inflammatory cytokines, oxidative stress markers, and CMKLR1 expression were evaluated. In vitro, LPS-stimulated HK-2 cells were treated with 1,25(OH)(2)D(3) with or without CMKLR1 overexpression to assess cytokines, cell viability, apoptosis, and oxidative stress. Four key biomarkers-CMKLR1, COL1A1, RPS19, and THBS1-were identified by machine learning, with CMKLR1 as the key target. In SA-AKI mice, 1,25(OH)(2)D(3) downregulated CMKLR1, improved renal function, and reduced inflammation and oxidative stress. In LPS-stimulated HK-2 cells, it dose-dependently suppressed cytokine release, restored cell viability, and alleviated oxidative stress, while CMKLR1 overexpression partially reversed these effects. CMKLR1 was identified as a key immune inflammation target in SA-AKI. 1,25(OH)(2)D(3) was protected against renal injury by suppressing CMKLR1, and mitigating inflammation, oxidative stress, and apoptosis, while CMKLR1 overexpression partially reversed these effects. These findings highlight CMKLR1 as a potential therapeutic target for SA-AKI. ?CMKLR1 as a Therapeutic Target: Vitamin D-Mediated Suppression of Infl(epmc).pdf DeepDyve Pubget Overpricing