Evidence map›Paper›PMID 31085163›Full record

ReviewTranslational research : the journal of laboratory and clinical medicine2019

Emerging strategies to disrupt the central TGF-β axis in kidney fibrosis.

Michael Rauchman, David Griggs

Abstract readReview
In one paragraph

Review in Translational research : the journal of laboratory and clinical medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

17 citing papers in PubMed, 32 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

2 authors at 2 institutions in 1 country.

Michael RauchmanDivision of Nephrology, Department of Medicine, Washington University School of Medicine, Saint Louis, Missouri; VA St. Louis Health Care System, Saint Louis, Missouri. Electronic address: mrauchma@wustl.edu.
David GriggsDepartment of Molecular Microbiology and Immunology, Edward A. Doisy Research Center, Saint Louis University, Saint Louis, Missouri. Electronic address: david.griggs@health.slu.edu.
Saint Louis University · USWashington University in St. Louis · US

Funding

Mechanisms and Treatment of Kidney FibrosisI01BX003674 · VA · ST. LOUIS VA MEDICAL CENTER · PI RAUCHMAN, MICHAEL I · 2018 to 2023
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BLRD VA I01 BX003674
6 · The paper itself

Abstract

Chronic kidney disease (CKD) affects more than 20 million people in the United States and the global burden of this disorder is increasing. Many affected individuals will progress to end stage kidney disease necessitating dialysis or transplantation. CKD is also a major independent contributor to the risk of cardiovascular morbidity and mortality. Tubulointerstitial fibrosis is a final common pathway for most causes of progressive CKD. Currently, there are no clinically available therapies targeting fibrosis that can slow the decline in kidney function. Although it has long been known that TGF-β signaling is a critical mediator of kidney fibrosis, translating this knowledge to the clinic has been challenging. In this review, we highlight some recent insights into the mechanisms of TGF-β signaling that target activation of this cytokine at the site of injury or selectively inhibit pro-fibrotic gene expression. Molecules directed at these targets hold the promise of attaining therapeutic efficacy while limiting toxicity seen with global inhibition of TGF-β. Kidney injury has profound epigenetic effects leading to altered expression of more than a thousand genes. We discuss how drugs targeting epigenetic modifications, some of which are in use for cancer therapy, have the potential to reprogram gene regulatory networks to favor adaptive repair and prevent fibrosis. The lack of reliable biomarkers of kidney fibrosis is a major limitation in designing clinical trials for testing CKD treatments. We conclude by reviewing recent advances in fibrosis biomarker development.

Indexed as

Signal TransductionDNA MethylationFibrosisHumansKidneyModels, BiologicalTransforming Growth Factor betaTransforming Growth Factor beta

Identifiers

PMID31085163
PMCPMC6850218
OpenAlexW2940874449

What OpenQuestion holds

Textmetadata
LicenceTDM
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.