In one paragraphArticle in American journal of physiology. Renal physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
2 · The registryThe trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
3 · Its place in the literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
5 · Who and what moneyAuthors and funding
11 authors.
Afaf SalibaCenter for Precision Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States.ORCID 0000-0003-2576-4069 Yidong ChenDepartment of Population Health Sciences, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States.
Jonathan W NelsonDivision of Nephrology and Hypertension, Department of Medicine, Keck School of Medicine of University of Southern California, Los Angeles, California, United States.ORCID 0000-0003-1456-9399 Abhinav VetchaCenter for Precision Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States.
Wei Wei WangDivision of Nephrology, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States.
Li KangDivision of Nephrology, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States.
Nagarjunachary RagiCenter for Precision Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States.ORCID 0000-0002-2009-525X Soumya MaityCenter for Precision Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States.
W Brian ReevesDivision of Nephrology, Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States.ORCID 0000-0001-5191-5866 Kumar SharmaCenter for Precision Medicine, University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States.ORCID 0000-0002-7550-8525 Funding
TISSUE CULTURE---COREP30CA054174 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Lei Zheng · 1991 to 2026
$59.1MPATHOBIOLOGY OF OCCLUSIVE VASCULAR DISEASET32HL007446 · NHLBI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Jean Chrisostome Bopassa · 1985 to 2026
$8.9MSpatial Multi-Omics to Profile Metabolic Pathways for Kidney DiseaseU01DK114920 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Christopher R Anderton, Kumar Sharma · 2022 to 2026
$3.9MNRSA Training Core (TL1)TL1TR002647 · NCATS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CHUN, YONG-HEE PATRICIA, FREI, CHRISTOPHER R. · 2018 to 2022
$1.8MIllumina NovaSeq 6000 Sequencing SystemS10OD030311 · OD · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI LAI, ZHAO · 2021 to 2021
$600kBLRD VA I01 BX001340DOD | MHS | Congressionally Directed Medical Research Programs (CDMRP) PR181598HHS | NIH | National Center for Advancing Translational Sciences (NCATS) TL1-TR002647HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) T32-HL007446HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) UO1DK114920NCATS NIH HHS TL1 TR002647NCI NIH HHS P30 CA054174NHLBI NIH HHS T32 HL007446NIDDK NIH HHS U01 DK114920NIH HHS S10 OD030311U.S. Department of Veterans Affairs (VA) I01BX001340
6 · The paper itselfAbstract
Methylthioadenosine phosphorylase (MTAP) is a key enzyme in purine metabolism that may influence cellular responses to injury. We evaluated the effects of prophylactic MTAP inhibition in mouse models of ischemia-reperfusion and cisplatin-induced acute kidney injury (AKI). MTAP inhibition was confirmed by the accumulation of methylthioadenosine. Treated mice showed reduced renal injury and decreased tubular damage. Transcriptomic analysis revealed protection from inflammatory and stress pathways while maintaining oxidative phosphorylation, fatty acid metabolism, and epithelial integrity-related genes. Analysis of human single-cell RNA sequencing data from the Kidney Precision Medicine Project indicated that MTAP is highly expressed in kidney injury marker-positive adaptive proximal tubule cells, which display both reparative and maladaptive features during AKI. These findings highlight MTAP as a potential therapeutic target for modulating injury responses in AKI.
Indexed as
Acute Kidney InjuryEnzyme InhibitorsKidney Tubules, ProximalPurine-Nucleoside PhosphorylaseReperfusion InjuryAnimalsCisplatinDisease Models, AnimalHumansMaleMiceMice, Inbred C57BL5'-methylthioadenosine phosphorylaseCisplatinEnzyme InhibitorsPurine-Nucleoside Phosphorylaseacute kidney injuryexperimental acute kidney injurymethylthioadenosine phosphorylaseprophylactic treatmentproximal tubules
Identifiers
PMID40602784
PMCPMC12501988
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