Evidence map›Paper›PMID 27550296›Full record

ReviewRheumatology (Oxford, England)2017

Transforming growth factor β activated kinase 1: a potential therapeutic target for rheumatic diseases.

Sabrina Fechtner, David A Fox, Salahuddin Ahmed

Open access · bronzeAbstract readReview
In one paragraph

Review in Rheumatology (Oxford, England), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

26 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. RepurposingACS omega · 2026
    Article
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  17. USP2-Related Cellular Signaling and Consequent Pathophysiological Outcomes.International journal of molecular sciences · 2021
    Review
  18. Article
  19. Article
  20. RIPK3: A New Player in Renal Fibrosis.Frontiers in cell and developmental biology · 2020
    Review
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

3 authors at 2 institutions in 1 country.

Sabrina FechtnerDepartment of Pharmaceutical Sciences, Washington State University College of Pharmacy, Spokane, WA.
David A FoxDepartment of Internal Medicine, Division of Rheumatology, University of Michigan Medical School, Ann Arbor, MI, USA.
Salahuddin AhmedDepartment of Pharmaceutical Sciences, Washington State University College of Pharmacy, Spokane, WA.
Washington State University Spokane · USUniversity of Michigan–Ann Arbor · US

Funding

Regulation of IL-6 mediated inflammation and tissue destruction by EGCGR01AR063104 · NIAMS · WASHINGTON STATE UNIVERSITY · PI AHMED, SALAH-UDDIN · 2013 to 2017
$1.7M
NIAMS NIH HHS R01 AR063104
6 · The paper itself

Abstract

Pro-inflammatory cytokines such as IL-1β, IL-6 and TNF-α are central regulators of autoinflammatory diseases. While targeting these cytokines has proven to be a successful clinical strategy, the long-term challenges such as drug resistance, lack of efficacy and poor clinical outcomes in some patients are some of the limitations faced by these therapies. This has ignited strategies to reduce inflammation by potentially targeting a variety of molecules, including cell surface receptors, signalling proteins and/or transcription factors to minimize cytokine-induced inflammation and tissue injury. In this regard, transforming growth factor β activated kinase 1 (TAK1) is activated in the inflammatory signal transduction pathways in response to IL-1β, TNF-α or toll-like receptor stimulation. Because of its ideal position upstream of mitogen-activated protein kinases and the IκB kinase complex in signalling cascades, targeting TAK1 may be an attractive strategy for treating diseases characterized by chronic inflammation. Here, we discuss the emerging role of TAK1 in mediating the IL-1β, TNF-α and toll-like receptor mediated inflammatory responses in diseases such as RA, OA, gout and SS. We also review evidence suggesting that TAK1 inhibition may have potential therapeutic value. Finally, we focus on the current status of the development of TAK1 inhibitors and suggest further opportunities for testing TAK1 inhibitors in rheumatic diseases.

Indexed as

Molecular Targeted TherapyAntirheumatic AgentsCytokinesFemaleHumansInflammation MediatorsInterleukin-1betaInterleukin-6MaleMAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesPrognosisRheumatic DiseasesTransforming Growth Factor betaAntirheumatic AgentsCytokinesInflammation MediatorsInterleukin-1betaInterleukin-6MAP Kinase Kinase Kinase 7MAP Kinase Kinase KinasesTransforming Growth Factor betagoutinflammationinhibitionosteoarthritisrheumatoid arthritisSjögren’s syndromeTAK1

Identifiers

PMID27550296
PMCPMC5850516
OpenAlexW2510049837

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.