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The anti-fibrotic drug pirfenidone inhibits liver fibrosis by targeting glrx

ABSTRACT: The anti-fibrotic drug pirfenidone inhibits liver fibrosis by targeting glrx

PROVIDER: PRJNA778750 | ENA |

REPOSITORIES: ENA

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The anti-fibrotic drug pirfenidone inhibits liver fibrosis by targeting glrx

Project description:Purpose: The goals of this study are to compare transcriptomes of mouse primary HSCs treated with PFD or vehicle by RNA-seq

2021-11-08 | GSE188420 | GEO

The anti-fibrotic drug pirfenidone inhibits liver fibrosis by targeting the small oxidoreductase glutaredoxin-1.

Project description: Not available

| S-EPMC8442864 | biostudies-literature

Redundant effects of Pirfenidone against fibroblast activation and severe fibrotic lung disease

Project description:Idiopathic Pulmonary Fibrosis (IPF) is a progressive chronic lung disease characterized by excess deposition of extracellular matrix (ECM) proteins in the lung. TGFα is a is a ligand for the epidermal growth factor receptor, and found elevated in several fibrotic lung diseases including IPF. Notably, lung-specific overexpression of TGFα alone in adult mice can cause progressive and extensive adventitial and subpleural fibrosis similar to IPF. Pirfenidone, an FDA approved drug has been shown to improve the decline in lung function in IPF patients. However, the mechanism of action of pirfenidone largely unknown. In the current study, we investigated the effects of pirfenidone using a mouse model of TGFα-induced pulmonary fibrosis and fibroblasts isolated from IPF lungs. Total lung transcriptome analysis suggest a significant overlap in dysregulated gene transcripts between TGFα model and IPF. In vivo studies demonstrate a significant improvement in lung function with pirfenidone therapy compared to vehicle-treated TGFα mice on Dox for six wks. However, pirfenidone treatment did not affect fibroproliferation, myofibroblast transformation, and ECM deposition during TGFα-induced pulmonary fibrosis. In summary, pirfenidone treatment improved lung function but had a limited or no effect on the expression of collagen, ECM genes, fibroproliferation and migration of lung-resident fibroblasts.

2022-06-01 | GSE199034 | GEO

Mesothelioma xenografts in nude mice: PBS treated versus pirfenidone treated

Project description:Background: Malignant mesothelioma is an aggressive cancer with poor prognosis. It is characterized by prominent extracellular matrix, mesenchymal tumor cell phenotypes and chemoresistance. In this study, the ability of pirfenidone to alter mesothelioma cell proliferation and migration as well as mesothelioma tumor microenvironment was evaluated. Pirfenidone is an anti-fibrotic drug used in the treatment of idiopathic pulmonary fibrosis and has also anti-proliferative activities. Aims: Transcriptional profiling using RNA sequencing of human mesothelioma xenograft tumors treated with PBS or pirfenidone. Aim was to compare extracellular matrix and fibrosis related genes. Results: Treatment of mice harboring mesothelioma xenografts with pirfenidone alone did not reduce tumor proliferation in vivo. However, pirfenidone modified the tumor microenvironment by reducing the expression of extracellular matrix associated genes. In addition, GREM1 expression was downregulated by pirfenidone in vivo. Conclusion: By reducing two major upregulated pathways in mesothelioma and by targeting tumor cells and the microenvironment pirfenidone may present a novel anti-fibrotic and anti-cancer adjuvant therapy for mesothelioma.

2018-12-14 | GSE113803 | GEO

Effect of pirfenidone on serum-stimulated human lung fibroblasts

Project description:Idiopathic pulmonary fibrosis (IPF) is an incurable lung disease with a poor prognosis. Fibroblasts and myofibroblasts are the key cells in the fibrotic process. Pirfenidone was approved as an anti-fibrotic drug for IPF treatment as it is able to slow disease progression. The mechanisms by which the drug acts on fibroblasts are not clear. Therefore, this study aims to examine the effects of pirfenidone on the human lung fibroblast (HLF) transcriptome in vitro.

2023-05-12 | GSE226249 | GEO

Redundant effects of Pirfenidone against fibroblast activation and severe fibrotic lung disease

Project description:Redundant effects of Pirfenidone against fibroblast activation and severe fibrotic lung disease

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The Multi-Modal Effect of the Anti-fibrotic Drug Pirfenidone on NSCLC.

Project description: Not available

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Fibrotic microtissue array to predict anti-fibrosis drug efficacy.

Project description: Not available

| S-EPMC5970268 | biostudies-literature

Spontaneous lung fibrosis resolution reveals novel anti-fibrotic regulators

Project description:Spontaneous lung fibrosis resolution reveals novel anti-fibrotic regulators

| PRJNA677893 | ENA

Effect of Pirfenidone on NSCLC [A549 1.5 mg/ml Pirf 24hrs]

Project description:Investigating the effect of Pirfenidone on NSCLC cells Although immune checkpoint and targeted therapies offer remarkable benefits for lung cancer treatment, some patients do not qualify for these regimens or do not exhibit consistent benefit. Provided that lung cancer appears to be driven by transforming growth factor beta signaling, we investigated the single drug potency of Pirfenidone, an approved drug for the treatment of lung fibrosis which is known to inhibit TGFB1 mRNA. Human A549 and H1975 lung adenocarcinoma cell lines were stimulated for 6h and 25h with 0.75 mg/ml or 1.5 mg/ml Pirfenidone or the respective volume of PBS as vehicle control. Total RNA was extracted and subjected to transcriptome analysis by microarrays.

2019-12-17 | GSE136934 | GEO

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