In one paragraphArticle in International journal of molecular sciences, 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
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
8 authors.
María Ángeles González-NicolásRenal Physiopathology Laboratory, Department of Nephrology, Instituto de Investigación Sanitaria Gregorio Marañón, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain.ORCID 0000-0002-3514-4616 Blanca HumanesRenal Physiopathology Laboratory, Department of Nephrology, Instituto de Investigación Sanitaria Gregorio Marañón, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain.
Raquel HerreroDepartment of Critical Care Medicine, Hospital Universitario de Getafe, 28905 Madrid, Spain.
Mario ArenillasAnimal Medicine and Surgery Department, Complutense University of Madrid, 28040 Madrid, Spain.ORCID 0000-0002-3315-7931 Beatriz LópezDepartment of Pathology, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain.
Antonio FerrueloCIBER de Enfermedades Respiratorias, Instituto de Investigación Carlos III, 28029 Madrid, Spain.
José Ángel LorenteDepartment of Critical Care Medicine, Hospital Universitario de Getafe, 28905 Madrid, Spain.ORCID 0000-0001-7679-9187 Alberto LázaroRenal Physiopathology Laboratory, Department of Nephrology, Instituto de Investigación Sanitaria Gregorio Marañón, Hospital General Universitario Gregorio Marañón, 28007 Madrid, Spain.ORCID 0000-0002-1095-679X Funding
Comunidad de Madrid CIFRA_COR-CM, 2022/BMD-7223Comunidad de Madrid EXOHEP2-CM, 2022/BMD-7409Fundación Mutua Madrileña XX Convocatoria de Ayudas a la Investigación en SaludSpanish Ministry of Economy and Competitiveness Instituto de Salud Carlos III-Fondo de Investigación en Salud ICI21/00111Spanish Ministry of Economy and Competitiveness Instituto de Salud Carlos III-Fondo de Investigación en Salud PI14/01195Spanish Ministry of Economy and Competitiveness Instituto de Salud Carlos III-Fondo de Investigación en Salud PI19/01091Spanish Ministry of Economy and Competitiveness Instituto de Salud Carlos III-Fondo de Investigación en Salud PI20/01577Spanish Ministry of Economy and Competitiveness Instituto de Salud Carlos III-Fondo de Investigación en Salud PI22/01611Spanish Ministry of Economy and Competitiveness Instituto de Salud Carlos III-Fondo de Investigación en Salud, RICORS2040-Renal RD24/0004/0023Spanish Ministry of Science and Innovation CPP2022-009633
6 · The paper itselfAbstract
Sepsis is a life-threatening condition caused by an abnormal host response to infection, leading to organ dysfunction and potentially death. Acute kidney injury (AKI) is a critical complication of sepsis. Various pathways, especially signaling through Toll-like receptors (TLRs) and the nucleotide-binding oligomerization domain, leucine-rich repeat and pyrin domain-containing protein 3 (NLRP3) inflammasome, contribute to inflammation and tissue damage. Cilastatin, a renal dehydropeptidase I inhibitor, has shown promise in protecting against AKI induced by nephrotoxic drugs. This study assessed cilastatin's effectiveness in preventing AKI and inflammation caused by sepsis and its impact on survival. Sepsis was induced in male
Indexed as
Acute Kidney InjuryCilastatinSepsisAnimalsBiomarkersBlood Urea NitrogenCreatinineDisease Models, AnimalKidneyMaleNLR Family, Pyrin Domain-Containing 3 ProteinRatsRats, Sprague-DawleyToll-Like Receptor 4BiomarkersCilastatinCreatinineNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, ratToll-Like Receptor 4acute kidney injurycilastatinCLPinflammationnephroprotectionsepsisTLR4
Identifiers
PMID40869248
PMCPMC12386316
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