Evidence map›Paper›PMID 30385721›Full record

ArticleJCI insight2018

TGF-β promotes fibrosis after severe acute kidney injury by enhancing renal macrophage infiltration.

Sungjin Chung, Jessica M Overstreet, Yan Li, Yinqiu Wang, Aolei Niu, Suwan Wang, Xiaofeng Fan, Kensuke Sasaki, Guan-Nan Jin, Stellor Nlandu Khodo and 3 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
7.3field-weighted citation impact, top 2% 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

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 115 citations in OpenAlex.

  1. Pooled it
  2. Article
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    Review
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  5. Fibrosis in Immune-Mediated and Autoimmune Disorders.Journal of clinical medicine · 2025
    Review
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13 more citing papers are in PubMed but not listed here.

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

13 authors at 1 institution in 2 countries.

Sungjin ChungDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Jessica M OverstreetDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Yan LiDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Yinqiu WangDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Aolei NiuDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Suwan WangDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Xiaofeng FanDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Kensuke SasakiDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Guan-Nan JinDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Stellor Nlandu KhodoDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Leslie GewinDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Ming-Zhi ZhangDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Raymond C HarrisDivision of Nephrology and Hypertension, Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
Vanderbilt University · US

Funding

The Role of the EGF Receptor in Acute and Chronic Renal InjuryR01DK051265 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RAYMOND C. HARRIS, Mingzhi Zhang · 1997 to 2026
$10.1M
The role of the innate immune cell cyclooxygenase/prostaglandin system in blood pressureregulationR01DK062794 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RAYMOND C. HARRIS, Mingzhi Zhang · 2003 to 2026
$9.4M
The Role of renal macrophages in recovery from renal injuryR01DK095785 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI RAYMOND C. HARRIS, Mingzhi Zhang · 2013 to 2026
$6.7M
Vanderbilt O'Brien Kidney Center - Core D - Clinical and Translational CoreP30DK114809 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI DE CAESTECKER, MARK P. · 2017 to 2021
$5.9M
TGF-beta Pathways that Protect Epithelia in Chronic Renal InjuryR01DK108968 · NIDDK · WASHINGTON UNIVERSITY · PI GEWIN, LESLIE S · 2016 to 2025
$3.7M
BLRD VA I01 BX003425NIDDK NIH HHS P30 DK114809NIDDK NIH HHS R01 DK051265NIDDK NIH HHS R01 DK062794NIDDK NIH HHS R01 DK095785NIDDK NIH HHS R01 DK108968
6 · The paper itself

Abstract

TGF-β signals through a receptor complex composed of 2 type I and 2 type II (TGF-βRII) subunits. We investigated the role of macrophage TGF-β signaling in fibrosis after AKI in mice with selective monocyte/macrophage TGF-βRII deletion (macrophage TGF-βRII-/- mice). Four weeks after injury, renal TGF-β1 expression and fibrosis were higher in WT mice than macrophage TGF-βRII-/- mice, which had decreased renal macrophages. The in vitro chemotactic response to f-Met-Leu-Phe was comparable between bone marrow-derived monocytes (BMMs) from WT and macrophage TGF-βRII-/- mice, but TGF-βRII-/- BMMs did not respond to TGF-β. We then implanted Matrigel plugs suffused with either f-Met-Leu-Phe or TGF-β1 into WT or macrophage TGF-βRII-/- mice. After 6 days, f-Met-Leu-Phe induced similar macrophage infiltration into the Matrigel plugs of WT and macrophage TGF-βRII-/- mice, but TGF-β induced infiltration only in WT mice. We further determined the number of labeled WT or TGF-βRII-/- BMMs infiltrating into WT kidneys 20 days after ischemic injury. There were more labeled WT BMMs than TGF-βRII-/- BMMs. Therefore, macrophage TGF-βRII deletion protects against the development of tubulointerstitial fibrosis following severe ischemic renal injury. Chemoattraction of macrophages to the injured kidney through a TGF-β/TGF-βRII axis is a heretofore undescribed mechanism by which TGF-β can mediate renal fibrosis during progressive renal injury.

Indexed as

Acute Kidney InjuryAnimalsBone Marrow CellsChemotactic FactorsFibrosisKidneyMacrophagesMaleMiceMice, TransgenicMonocytesN-Formylmethionine Leucyl-PhenylalanineReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IITransforming Growth Factor betaTransforming Growth Factor beta1Chemotactic FactorsN-Formylmethionine Leucyl-PhenylalanineReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IITransforming Growth Factor betaTransforming Growth Factor beta1ChemokinesFibrosisMacrophagesNephrology

Identifiers

PMID30385721
PMCPMC6238749
OpenAlexW2899136988

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.