Tranilast: A review of its therapeutic applications

Darakhshan, Sara; Pour, Ali Bidmeshki

doi:10.1016/j.phrs.2014.10.009

Cited by 247 publications

(234 citation statements)

References 183 publications

Supporting

Mentioning

225

Contrasting

Unclassified

Order By: Relevance

“…Hahn et al demonstrated that keloid keratinocytes exhibit adhesion abnormalities and display a transcriptional signature reminiscent of cells undergoing epithelial-mesenchymal transition (EMT). A critical mediator in this process is TGF-β1 [29], the factor whose expression is downregulated in many cells by tranilast [1,31]. In keloids, keratinocytes promote proliferation, inhibit apoptosis of the underlying fibroblasts and upregulate TGF-β1 expression -the key regulator of fibrotic processes [30].…”

Section: Suzawa Et Al Revealed That Tranilast Selective Inhibition Omentioning

confidence: 99%

“…It blocks degranulation of mast cells and basophils [1,2] and inhibits the release of inflammatory mediators such as histamine, leukotrienes, prostaglandins and platelet-activating factor (PAF), which are produced by mast cells and basophils [3].…”

Section: Introductionmentioning

confidence: 99%

“…Because of the lack of effective WPROWADZENIE Tranilast (Rizaben), pochodna kwasu antranilowego (kwasu N-(3',4'-demetoksycynamoilo)-antranilowego), jest lekiem przeciwalergicznym. Blokuje degranulację mastocytów i granulocytów zasadochłonnych [1,2] oraz hamuje wydzielanie mediatorów zapalnych, m.in. histaminy, leukotrienów, prostaglandyn oraz czynnika aktywującego płytki krwi (PAF), wytwarzanych przez mastocyty i granulocyty zasadochłonne [3].…”

Section: Introductionunclassified

“…The mechanism of antifibrotic action of the drug is not fully understood. Studies suggest that the antifibrotic effect of tranilast relies on collagen synthesis inhibition and inhibition of both transforming growth factor β (TGF-β) expression and TGF-β action [1,2,[4][5][6].…”

Section: Introductionmentioning

confidence: 99%

“…Mechanizm działania przeciwfibrotycznego leku nie jest w pełni poznany. Badania sugerują, że właściwo-ści przeciwfibrotyczne tranilastu wynikają z blokowania syntezy kolagenu oraz hamowania ekspresji i działania transformującego czynnika wzrostu β (TGF-β) [1,2,[4][5][6].…”

Section: Introductionunclassified

See 4 more Smart Citations

The effect of tranilast on fibroblast activation protein α (FAP-α) expression in normal and keloid fibroblasts in vitro

Antończak¹,

Jurzak²,

Adamczyk³

et al. 2017

View full text Add to dashboard Cite

Introduction. Tranilast (N-(3',4'-demethoxycinnamoyl)-anthranilic acid)is an anti-allergic drug. Its mechanism of action is based on the inhibition of antigen-induced release of chemical mediators from mast cells and basophils. It also reveals antifibroproliferative activities. These properties of tranilast are used in the treatment of hypertrophic scars and keloids. Keloids are characterized by incorrect extracellular matrix components turnover. Fibroblasts derived from keloids reveal overproduction of collagen type I and decreased degradation of extracellular matrix in comparison with normal fibroblasts. Fibroblast activation protein α (FAP-α) may play an important role in remodeling of extracellular matrix and the invasive properties of keloids. Objective. In the present study, the effect of tranilast on expression of FAP-α gene and its protein was evaluated in normal human dermal fibroblasts and fibroblasts derived from keloids cultured in vitro. Materials and methods. In the first stage of the study, the influence of tranilast on cell viability was estimated. The second stage of the study included the quantitative evaluation of FAP-α mRNA expression in normal and keloid fibroblasts treated with tranilast. The third stage of the study comprised fibroblast activation protein α expression analysis in the examined cells treated with tranilast. Results and conclusions. The expression of FAP-α gene and fibroblast activation protein α is higher in keloid fibroblasts. Tranilast at concentrations of 3 μM and 30 μM up-regulated mRNA FAP-α expression in normal fibroblasts but did not influence keloid fibroblasts. The drug, at concentrations of 30 μM and 300 μM up-regulated fibroblast activation protein α expression in normal fibroblasts and did not influence keloid fibroblasts. Tranilast antiproliferative effect is not associated with FAP-α expression in keloid fibroblasts. Original article/Praca oryginalnaThe effect of tranilast on fibroblast activation protein α (FAP-α) expression in normal and keloid fibroblasts in vitro Wpływ tranilastu na ekspresję białka aktywującego fibroblasty α (FAP-α) w fibroblastach prawidłowych oraz fibroblastach keloidowych in vitro

show abstract

Section: Suzawa Et Al Revealed That Tranilast Selective Inhibition Omentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionunclassified

Section: Introductionmentioning

confidence: 99%

Section: Introductionunclassified

See 3 more Smart Citations

The effect of tranilast on fibroblast activation protein α (FAP-α) expression in normal and keloid fibroblasts in vitro

Antończak¹,

Jurzak²,

Adamczyk³

et al. 2017

View full text Add to dashboard Cite

show abstract

Fibrosis‐on‐Chip: A Guide to Recapitulate the Essential Features of Fibrotic Disease

Streutker,

Devamoglu,

Vonk

et al. 2024

Adv Healthcare Materials

View full text Add to dashboard Cite

Fibrosis, which is primarily marked by excessive extracellular matrix (ECM) deposition, is a pathophysiological process associated with many disorders, which ultimately leads to organ dysfunction and poor patient outcomes. Despite the high prevalence of fibrosis, currently there exist few therapeutic options, and importantly, there is a paucity of in vitro models to accurately study fibrosis. This review discusses the multifaceted nature of fibrosis from the viewpoint of developing organ‐on‐chip (OoC) disease models, focusing on five key features: the ECM component, inflammation, mechanical cues, hypoxia and vascularization. We explore the potential of OoC technology for better modeling these features in the context of studying fibrotic diseases and emphasize the interplay between various key features. We review how organ‐specific fibrotic diseases have been modeled in OoC platforms, which elements have been included in these existing models, and we highlight avenues for novel research directions. Finally, we conclude with a perspective section on how to address the current gap with respect to the inclusion of multiple features to yield more sophisticated and relevant models of fibrotic diseases in an OoC format.This article is protected by copyright. All rights reserved

show abstract

Tau‐induced deficits in nonsense‐mediated mRNA decay contribute to neurodegeneration

Zuniga

Levy

Ramirez

et al. 2022

Alzheimer's & Dementia

View full text Add to dashboard Cite

Introduction While brains of patients with Alzheimer's disease and related tauopathies have evidence of altered RNA processing, we lack a mechanistic understanding of how altered RNA processing arises in these disorders and if such changes are causally linked to neurodegeneration. Methods Using Drosophila melanogaster models of tauopathy, we find that overall activity of nonsense‐mediated mRNA decay (NMD), a key RNA quality‐control mechanism, is reduced. Genetic manipulation of NMD machinery significantly modifies tau‐induced neurotoxicity, suggesting that deficits in NMD are causally linked to neurodegeneration. Mechanistically, we find that deficits in NMD are a consequence of aberrant RNA export and RNA accumulation within nuclear envelope invaginations in tauopathy. We identify a pharmacological activator of NMD that suppresses neurodegeneration in tau transgenic Drosophila, indicating that tau‐induced deficits in RNA quality control are druggable. Discussion Our studies suggest that NMD activators should be explored for their potential therapeutic value to patients with tauopathies.

show abstract

Tranilast: A review of its therapeutic applications

Cited by 247 publications

References 183 publications

The effect of tranilast on fibroblast activation protein α (FAP-α) expression in normal and keloid fibroblasts in vitro

The effect of tranilast on fibroblast activation protein α (FAP-α) expression in normal and keloid fibroblasts in vitro

Fibrosis‐on‐Chip: A Guide to Recapitulate the Essential Features of Fibrotic Disease

Tau‐induced deficits in nonsense‐mediated mRNA decay contribute to neurodegeneration

Contact Info

Product

Resources

About