Evidence map›Paper›PMID 31813254›Full record

ArticleAmerican journal of physiology. Renal physiology2020

TAK1 deficiency attenuates cisplatin-induced acute kidney injury.

Jun Zhou, Changlong An, Xiaogao Jin, Zhaoyong Hu, Robert L Safirstein, Yanlin Wang

Open access · bronzeAbstract 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 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  8. Pro-Inflammatory Signalling PRRopels Cisplatin-Induced Toxicity.International journal of molecular sciences · 2022
    Review
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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

6 authors at 4 institutions in 2 countries.

Jun ZhouSection of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas.
Changlong AnSection of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas.
Xiaogao JinSection of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas.
Zhaoyong HuSection of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas.ORCID 0000-0003-4171-3587
Robert L SafirsteinRenal Section, Veterans Affairs Connecticut Healthcare System, West Haven, Connecticut.
Yanlin WangSection of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas.
Baylor College of Medicine · USUniversity of Connecticut · USGuilin Medical University · CNVA Connecticut Healthcare System · US

Funding

Cellular and Molecular Mechanisms of Renal FibrosisR01DK095835 · NIDDK · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI WANG, YANLIN · 2012 to 2021
$3.2M
Targeting histone deacetylase 3 for chronic kidney diseaseI01BX002650 · VA · VA CONNECTICUT HEALTHCARE SYSTEM · PI YANLIN WANG · 2016 to 2026
–
BLRD VA I01 BX002650NIDDK NIH HHS R01 DK095835
6 · The paper itself

Abstract

Cisplatin can cause acute kidney injury (AKI), but the molecular mechanisms are not well understood. The objective of the present study was to examine the role of transforming growth factor-β-activated kinase-1 (TAK1) in the pathogenesis of cisplatin-induced AKI. Wild-type mice and proximal tubule TAK1-deficient mice were treated with vehicle or cisplatin. Compared with wild-type control mice, proximal tubule TAK1-deficient mice had less severe kidney dysfunction, tubular damage, and apoptosis after cisplatin-induced AKI. Furthermore, conditional disruption of TAK1 in proximal tubular epithelial cells reduced caspase-3 activation, proinflammatory molecule expression, and JNK phosphorylation in the kidney in cisplatin-induced AKI. Taken together, cisplatin activates TAK1-JNK signaling pathway to promote tubular epithelial cell apoptosis and inflammation in cisplatin-induced AKI. Targeting TAK1 could be a novel therapeutic strategy against cisplatin-induced AKI.

Indexed as

Acute Kidney InjuryAnimalsAntineoplastic AgentsApoptosisCisplatinEpithelial CellsKidneyMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesMiceMice, KnockoutPhosphorylationAntineoplastic AgentsCisplatinMAP Kinase Kinase Kinase 7MAP Kinase Kinase Kinasesacute kidney injuryapoptosischemokinesc-Jun NH2-terminal kinasecytokinestransforming growth factor-β-activated kinase-1

Identifiers

PMID31813254
PMCPMC6985823
OpenAlexW2996155802

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.