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Review
. 2024 Aug 20:137:112423.
doi: 10.1016/j.intimp.2024.112423. Epub 2024 Jun 10.

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

Gaelle Massoud  1 , Maclaine Parish  1 , Dana Hazimeh  1 , Pamela Moukarzel  2 , Bhuchitra Singh  1 , Kamaria C Cayton Vaught  1 , James Segars  3 , Md Soriful Islam  4
Affiliations
Review

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

Gaelle Massoud et al. Int Immunopharmacol. .

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.

Keywords: Cardiac fibrosis; Fibrosis; Inflammation; Keloids and hypertrophic scars; Liver fibrosis; Pulmonary fibrosis; Renal fibrosis; Scleroderma; Tranilast; Uterine fibroids.

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Conflict of interest statement

Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Figures

Figure 1.
Figure 1.
Schematic representation of inflammation and fibrosis. Created with BioRender.com.
Figure 2.
Figure 2.
Schematic representation of the effect of tranilast on fibrotic diseases. Created with BioRender.com.
Figure 3.
Figure 3.
Schematic representation of the effect of tranilast on uterine fibroids. Created with BioRender.com.
Figure 4.
Figure 4.
Schematic representation of the signaling pathways inhibited by tranilast in fibrotic conditions. Created with BioRender.com.
See this image and copyright information in PMC

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References

    1. Banerjee S, Biehl A, Gadina M, Hasni S, Schwartz DM, 2017. JAK-STAT signaling as a target for inflammatory and autoimmune diseases: current and future prospects. Drugs 77, 521–546. - PMC - PubMed
    1. Bataller R, Brenner DA, 2005. Liver fibrosis. J. Clin. Invest 115, 209–218. - PMC - PubMed
    1. Berman B, Maderal A, Raphael B, 2017. Keloids and hypertrophic scars: pathophysiology, classification, and treatment. Dermatol Surg 43 Suppl 1, S3–S18. - PubMed
    1. Border WA, Noble NA, 1998. Interactions of transforming growth factor-β and angiotensin II in renal fibrosis. Hypertension 31, 181–188. - PubMed
    1. Chen L, Deng H, Cui H, Fang J, Zuo Z, Deng J, Li Y, Wang X, Zhao L, 2018. Inflammatory responses and inflammation-associated diseases in organs. Oncotarget 9, 7204–7218. - PMC - PubMed

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