Evidence map›Paper›PMID 32200666›Full record

ArticleAmerican journal of physiology. Renal physiology2020

Increased fibrotic signaling in a murine model for intra-arterial contrast-induced acute kidney injury.

Amit Sharma, Sreenivasulu Kilari, Chuanqi Cai, Michael L Simeon, Sanjay Misra

Open access · hybridAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.0field-weighted citation impact, top 25% of its field
1 · What the graph read from it

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 registry

The 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 literature

Who cites it

7 citing papers in PubMed, 8 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Amit SharmaVascular and Interventional Radiology Translational Laboratory, Department of Radiology, Mayo Clinic, Rochester, Minnesota.
Sreenivasulu KilariVascular and Interventional Radiology Translational Laboratory, Department of Radiology, Mayo Clinic, Rochester, Minnesota.
Chuanqi CaiVascular and Interventional Radiology Translational Laboratory, Department of Radiology, Mayo Clinic, Rochester, Minnesota.
Michael L SimeonVascular and Interventional Radiology Translational Laboratory, Department of Radiology, Mayo Clinic, Rochester, Minnesota.
Sanjay MisraVascular and Interventional Radiology Translational Laboratory, Department of Radiology, Mayo Clinic, Rochester, Minnesota.ORCID 0000-0001-5662-796X
Mayo Clinic in Arizona · USMayo Clinic · USUnion Hospital · CN

Funding

The Role of Hypoxia In Venous Neointimal Hyperplasia In Hemodialysis GraftsR01HL098967 · NHLBI · MAYO CLINIC ROCHESTER · PI Sanjay Misra · 2010 to 2026
$10.4M
Regulatory gene-chemokine networks in the formation of hemodialysis AVF stenosisR01DK107870 · NIDDK · MAYO CLINIC ROCHESTER · PI KUMAR, RAJIV, MISRA, SANJAY · 2017 to 2019
$716k
Regulatory gene-chemokine networks in the formation of hemodialysis AVF stenosisR56DK107870 · NIDDK · MAYO CLINIC ROCHESTER · PI KUMAR, RAJIV, MISRA, SANJAY · 2020 to 2020
$103k
NHLBI NIH HHS R01 HL098967NIDDK NIH HHS R01 DK107870NIDDK NIH HHS R56 DK107870
6 · The paper itself

Abstract

Contrast-induced acute kidney injury (CI-AKI) is a vexing problem, and more than 70 million patients undergo studies using iodinated contrast. The molecular mechanisms responsible for CI-AKI are poorly understood. The goal of the present article was to determine the role of transforming growth factor-β1 (TGF-β1)/mothers against decapentaplegic homolog (SMAD)3 and associated collagen expression in a murine model of intra-arterial CI-AKI. The murine model of CI-AKI after intra-arterial contrast agent administration was created by first performing a partial nephrectomy to induce chronic kidney disease. Twenty-eight days later, 100 μL of contrast agent [iodixanol (320 mg/mL)] or saline were administered via the carotid artery. Two days after contrast administration, compared with saline, average serum creatinine was significantly elevated (

Indexed as

Contrast MediaTriiodobenzoic AcidsAcute Kidney InjuryAnimalsApoptosisCarotid ArteriesCell HypoxiaCell ProliferationCollagenDisease Models, AnimalFibrosisGene Expression RegulationHypoxia-Inducible Factor 1, alpha SubunitInjections, Intra-ArterialKidneyMaleCollagenContrast MediaHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitiodixanolReceptor, Transforming Growth Factor-beta Type IReceptor, Transforming Growth Factor-beta Type IISmad3 ProteinSmad3 protein, mouseTgfb1 protein, mouseTgfbr1 protein, mouseTgfbr2 protein, mouseTransforming Growth Factor beta1Triiodobenzoic Acidsanimal modelscontrastcreatininekidneykidney injury molecule-1postcontrast acute kidney injurytransforming growth factor-β1/SMAD3 signaling

Identifiers

PMID32200666
PMCPMC7294333
OpenAlexW3012718971

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.