Evidence map›Paper›PMID 31736350›Full record

ArticleAmerican journal of physiology. Renal physiology2020

TNF-α in T lymphocytes attenuates renal injury and fibrosis during nephrotoxic nephritis.

Yi Wen, Nathan P Rudemiller, Jiandong Zhang, Taylor Robinette, Xiaohan Lu, Jiafa Ren, Jamie R Privratsky, Sergei A Nedospasov, Steven D Crowley

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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

22 citing papers in PubMed, 29 citations in OpenAlex.

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  7. Targeted inhibition of Gus-expressingActa pharmaceutica Sinica. B · 2024
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  12. Tumor Necrosis Factor-Mediators of inflammation · 2023
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  18. Review
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  20. Article
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

9 authors at 4 institutions in 2 countries.

Yi WenDivision of Nephrology, Department of Medicine, Durham Veterans Affairs and Duke University Medical Center, Durham, North Carolina.
Nathan P RudemillerDivision of Nephrology, Department of Medicine, Durham Veterans Affairs and Duke University Medical Center, Durham, North Carolina.
Jiandong ZhangDivision of Nephrology, Department of Medicine, Durham Veterans Affairs and Duke University Medical Center, Durham, North Carolina.
Taylor RobinetteDivision of Nephrology, Department of Medicine, Durham Veterans Affairs and Duke University Medical Center, Durham, North Carolina.
Xiaohan LuDivision of Nephrology, Department of Medicine, Durham Veterans Affairs and Duke University Medical Center, Durham, North Carolina.
Jiafa RenDivision of Nephrology, Department of Medicine, Durham Veterans Affairs and Duke University Medical Center, Durham, North Carolina.
Jamie R PrivratskyDepartment of Anesthesiology, Durham Veterans Affairs and Duke University Medical Center, Durham, North Carolina.
Sergei A NedospasovLaboratory of Molecular Immunology, Engelhardt Institute of Molecular Biology and Lomonosov Moscow State University, Moscow, Russia.
Steven D CrowleyDivision of Nephrology, Department of Medicine, Durham Veterans Affairs and Duke University Medical Center, Durham, North Carolina.
Duke Medical Center · USDuke University Hospital · USDurham VA Medical Center · USLomonosov Moscow State University · RU

Funding

Role of Dendritic Cell-mediated T Cell Activation in Salt-sensitive HypertensionR01HL128355 · NHLBI · DUKE UNIVERSITY · PI CROWLEY, STEVEN D · 2016 to 2019
$1.9M
The interleukin-1 receptor regulates crosstalk between myeloid and renal tubular cells in hypertensionR01DK118019 · NIDDK · DUKE UNIVERSITY · PI CROWLEY, STEVEN D · 2019 to 2022
$1.7M
BLRD VA I01 BX000893NHLBI NIH HHS R01 HL128355NIDDK NIH HHS R01 DK118019
6 · The paper itself

Abstract

Nephrotoxic serum nephritis (NTN) models immune-mediated human glomerulonephritis and culminates in kidney inflammation and fibrosis, a process regulated by T lymphocytes. TNF-α is a key proinflammatory cytokine that contributes to diverse forms of renal injury. Therefore, we posited that TNF-α from T lymphocytes may contribute to NTN pathogenesis. Here, mice with T cell-specific deletion of TNF-α (TNF TKO) and wild-type (WT) control mice were subjected to the NTN model. At 14 days after NTN, kidney injury and fibrosis were increased in kidneys from TNF TKO mice compared with WT mice. PD1

Indexed as

AnimalsDisease Models, AnimalFibrosisGlomerulonephritisInterleukin-17KidneyMiceMice, KnockoutT-LymphocytesTumor Necrosis Factor-alphaInterleukin-17Tumor Necrosis Factor-alphacytokinenephritisT lymphocytetumor necrosis factor-α

Identifiers

PMID31736350
PMCPMC6985827
OpenAlexW2984283555

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.