Aspirin alleviates pulmonary fibrosis through PI3K/AKT/mTOR-mediated autophagy pathway

[Jam]

Aspirin alleviates pulmonary fibrosis through PI3K/AKT/mTOR-mediated autophagy pathway

Idiopathic pulmonary fibrosis (IPF) is a chronic and irreversible lung disease with limited therapeutic options. Aspirin can alleviate liver, kidney, …

www.sciencedirect.com

Highlights​

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Aspirin inhibits pulmonary fibrosis in lung fibroblasts and mice.
•
Aspirin induces autophagy.
•
Aspirin may block fibroblasts differentiation by inducing autophagy.
•
Aspirin induces autophagy by inhibiting PI3K/AKT/mTOR pathway.
•
Aspirin ameliorates pulmonary fibrosis through a PI3K/AKT/mTOR-dependent autophagy pathway.

Abstract​

Idiopathic pulmonary fibrosis (IPF) is a chronic and irreversible lung disease with limited therapeutic options. Aspirin can alleviate liver, kidney, and cardiac fibrosis. However, its role in lung fibrosis is unclear. This study aims to investigate the effects of aspirin on lung fibroblast differentiation and pulmonary fibrosis. TGF-β1-induced human embryonic lung fibroblasts, IPF lung fibroblasts, and bleomycin-induced lung fibrosis mouse model were used in this study. The results showed that aspirin significantly decreased the expression of Collagen 1A1, Fibronectin, Alpha-smooth muscle actin, and equestosome1, and increased the ratio of light chain 3 beta II/I and the number of autophagosome in vivo and in vitro; reduced bleomycin-induced lung fibrosis. Aspirin also decreased the ratios of phosphorylated phosphatidylinositol 3 kinase (p-PI3K)/PI3K, protein kinase B (p-AKT)/AKT, and mechanistic target of rapamycin (p-mTOR)/mTOR in vitro. Autophagy inhibitor 3-methyladenine, bafilomycin-A1, and AKT activator SC-79 abrogated the effects of aspirin. These findings indicate that aspirin ameliorates pulmonary fibrosis through a PI3K/AKT/mTOR-dependent autophagy pathway.

 

[Inaut]

Thanks @Jam

 

[area51puy]

Good find

 

[Regina]

Aspirin alleviates pulmonary fibrosis through PI3K/AKT/mTOR-mediated autophagy pathway

Idiopathic pulmonary fibrosis (IPF) is a chronic and irreversible lung disease with limited therapeutic options. Aspirin can alleviate liver, kidney, …

www.sciencedirect.com

Highlights​

•
Aspirin inhibits pulmonary fibrosis in lung fibroblasts and mice.
•
Aspirin induces autophagy.
•
Aspirin may block fibroblasts differentiation by inducing autophagy.
•
Aspirin induces autophagy by inhibiting PI3K/AKT/mTOR pathway.
•
Aspirin ameliorates pulmonary fibrosis through a PI3K/AKT/mTOR-dependent autophagy pathway.

Abstract​

Idiopathic pulmonary fibrosis (IPF) is a chronic and irreversible lung disease with limited therapeutic options. Aspirin can alleviate liver, kidney, and cardiac fibrosis. However, its role in lung fibrosis is unclear. This study aims to investigate the effects of aspirin on lung fibroblast differentiation and pulmonary fibrosis. TGF-β1-induced human embryonic lung fibroblasts, IPF lung fibroblasts, and bleomycin-induced lung fibrosis mouse model were used in this study. The results showed that aspirin significantly decreased the expression of Collagen 1A1, Fibronectin, Alpha-smooth muscle actin, and equestosome1, and increased the ratio of light chain 3 beta II/I and the number of autophagosome in vivo and in vitro; reduced bleomycin-induced lung fibrosis. Aspirin also decreased the ratios of phosphorylated phosphatidylinositol 3 kinase (p-PI3K)/PI3K, protein kinase B (p-AKT)/AKT, and mechanistic target of rapamycin (p-mTOR)/mTOR in vitro. Autophagy inhibitor 3-methyladenine, bafilomycin-A1, and AKT activator SC-79 abrogated the effects of aspirin. These findings indicate that aspirin ameliorates pulmonary fibrosis through a PI3K/AKT/mTOR-dependent autophagy pathway.

 

[area51puy]

Aspirin Alleviates Cardiac Fibrosis In Mice By Inhibiting Autophagy

Aspirin alleviates cardiac fibrosis in mice by inhibiting autophagy. - PubMed - NCBI Acta Pharmacol Sin. 2017 Apr;38(4):488-497. doi: 10.1038/aps.2016.143. Epub 2017 Feb 20. Aspirin alleviates cardiac fibrosis in mice by inhibiting autophagy. Liu PP1, Liu HH2, Sun SH3, Shi XX2, Yang WC2, Su...

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