Evidence map›Paper›PMID 38861914›Full record

ReviewInternational immunopharmacology2024

Unlocking the potential of tranilast: Targeting fibrotic signaling pathways for therapeutic benefit.

Gaelle Massoud, Maclaine Parish, Dana Hazimeh, Pamela Moukarzel, Bhuchitra Singh, Kamaria C Cayton Vaught, James Segars, Md Soriful Islam

Abstract readReview
In one paragraph

Review in International immunopharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
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

15 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Recent advances in biomarkers for cardiac fibrosis.Frontiers in cardiovascular medicine · 2026
    Review
  10. Article
  11. Comprehensive Update on Keloid Management.Archives of plastic surgery · 2026
    Article
  12. Article
  13. Review
  14. Review
  15. 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

8 authors.

Gaelle MassoudDepartment of Gynecology and Obstetrics, Division of Reproductive Sciences & Women's Health Research, Johns Hopkins Medicine, Baltimore, MD 21205, USA.
Maclaine ParishDepartment of Gynecology and Obstetrics, Division of Reproductive Sciences & Women's Health Research, Johns Hopkins Medicine, Baltimore, MD 21205, USA.
Dana HazimehDepartment of Gynecology and Obstetrics, Division of Reproductive Sciences & Women's Health Research, Johns Hopkins Medicine, Baltimore, MD 21205, USA.
Pamela MoukarzelAmerican University of Beirut Medical Center, Faculty of Medicine, Riad El Solh, Beirut, Lebanon.
Bhuchitra SinghDepartment of Gynecology and Obstetrics, Division of Reproductive Sciences & Women's Health Research, Johns Hopkins Medicine, Baltimore, MD 21205, USA.
Kamaria C Cayton VaughtDepartment of Gynecology and Obstetrics, Division of Reproductive Sciences & Women's Health Research, Johns Hopkins Medicine, Baltimore, MD 21205, USA.
James SegarsDepartment of Gynecology and Obstetrics, Division of Reproductive Sciences & Women's Health Research, Johns Hopkins Medicine, Baltimore, MD 21205, USA. Electronic address: jsegars2@jhmi.edu.
Md Soriful IslamDepartment of Gynecology and Obstetrics, Division of Reproductive Sciences & Women's Health Research, Johns Hopkins Medicine, Baltimore, MD 21205, USA. Electronic address: mislam18@jhmi.edu.

Funding

Role of senescent cells in uterine fibroid pathogenesisR01HD111243 · NICHD · JOHNS HOPKINS UNIVERSITY · PI Mostafa A. Borahay, JENNIFER H ELISSEEFF · 2023 to 2026
$3.2M
NICHD NIH HHS R01 HD111243
6 · The paper itself

Abstract

Fibrosis is the excessive deposition of extracellular matrix in an organ or tissue that results from an impaired tissue repair in response to tissue injury or chronic inflammation. The progressive nature of fibrotic diseases and limited treatment options represent significant healthcare challenges. Despite the substantial progress in understanding the mechanisms of fibrosis, a gap persists translating this knowledge into effective therapeutics. Here, we discuss the critical mediators involved in fibrosis and the role of tranilast as a potential antifibrotic drug to treat fibrotic conditions. Tranilast, an antiallergy drug, is a derivative of tryptophan and has been studied for its role in various fibrotic diseases. These include scleroderma, keloid and hypertrophic scars, liver fibrosis, renal fibrosis, cardiac fibrosis, pulmonary fibrosis, and uterine fibroids. Tranilast exerts antifibrotic effects by suppressing fibrotic pathways, including TGF-β, and MPAK. Because it disrupts fibrotic pathways and has demonstrated beneficial effects against keloid and hypertrophic scars, tranilast could be used to treat other conditions characterized by fibrosis.

Indexed as

Fibrosisortho-AminobenzoatesSignal TransductionAnimalsAntifibrotic AgentsHumansKeloidTransforming Growth Factor betaAntifibrotic Agentsortho-AminobenzoatestranilastTransforming Growth Factor betaCardiac fibrosisFibrosisInflammationKeloids and hypertrophic scarsLiver fibrosisPulmonary fibrosisRenal fibrosisSclerodermaTranilastUterine fibroids

Identifiers

PMID38861914
PMCPMC11245748

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.