Evidence map›Paper›PMID 24740541›Full record

ReviewAmerican journal of physiology. Cell physiology2014

Cellular mechanisms of tissue fibrosis. 8. Current and future drug targets in fibrosis: focus on Rho GTPase-regulated gene transcription.

Pei-Suen Tsou, Andrew J Haak, Dinesh Khanna, Richard R Neubig

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Cell physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

56 citing papers in PubMed, 82 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Targeting Fibrosis: From Molecular Mechanisms to Advanced Therapies.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Relaxin in fibrotic ligament diseases: Its regulatory role and mechanism.Frontiers in cell and developmental biology · 2023
    Review
  16. Article
  17. Rho/SRF Inhibitor Modulates Mitochondrial Functions.International journal of molecular sciences · 2022
    Article
  18. Article
  19. Article
  20. 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

4 authors at 2 institutions in 1 country.

Pei-Suen TsouDivision of Rheumatology, Department of Internal Medicine, University of Michigan Scleroderma Program, Ann Arbor, Michigan;
Andrew J HaakDepartment of Pharmacology, University of Michigan Medical Center, Ann Arbor, Michigan; and.
Dinesh KhannaDivision of Rheumatology, Department of Internal Medicine, University of Michigan Scleroderma Program, Ann Arbor, Michigan;
Richard R NeubigDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan RNeubig@msu.edu.
University of Michigan–Ann Arbor · USMichigan State University · US

Funding

TRAINING OF ARTHRITIS RESEARCH SCIENTISTST32AR007080 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Jason Knight · 1986 to 2026
$6.3M
Outcomes Research in Rheumatic DiseasesK24AR063120 · NIAMS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KHANNA, DINESH · 2012 to 2022
$1.6M
NIAMS NIH HHS K24 AR063120NIAMS NIH HHS K24 AR-063120-02NIAMS NIH HHS T32 AR007080
6 · The paper itself

Abstract

Tissue fibrosis occurs with excessive extracellular matrix deposition from myofibroblasts, resulting in tissue scarring and inflammation. It is driven by multiple mediators, such as the G protein-coupled receptor ligands lysophosphatidic acid and endothelin, as well as signaling by transforming growth factor-β, connective tissue growth factor, and integrins. Fibrosis contributes to 45% of deaths in the developed world. As current therapeutic options for tissue fibrosis are limited and organ transplantation is the only effective treatment for end-stage disease, there is an imminent need for efficacious antifibrotic therapies. This review discusses the various molecular pathways involved in fibrosis. It highlights the Rho GTPase signaling pathway and its downstream gene transcription output through myocardin-related transcription factor and serum response factor as a convergence point for targeting this complex set of diseases.

Indexed as

Drug DesignTranscription, GeneticAnimalsConnective Tissue DiseasesEnzyme InhibitorsFibrosisHumansMolecular Targeted TherapyMyofibroblastsrho GTP-Binding ProteinsSerum Response FactorSignal TransductionEnzyme Inhibitorsrho GTP-Binding ProteinsSerum Response Factordrug developmentfibrosisgene transcriptionRho GTPasetherapeutics

Identifiers

PMID24740541
PMCPMC4080186
OpenAlexW2033122114

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.