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Cellular Senescence: A Troy Horse in Pulmonary Fibrosis

Overview
Journal Int J Mol Sci
Publisher MDPI
Date 2023 Nov 25
PMID 38003600
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Abstract

Pulmonary fibrosis (PF) is a chronic interstitial lung disease characterized by myofibroblast abnormal activation and extracellular matrix deposition. However, the pathogenesis of PF remains unclear, and treatment options are limited. Epidemiological studies have shown that the average age of PF patients is estimated to be over 65 years, and the incidence of the disease increases with age. Therefore, PF is considered an age-related disease. A preliminary study on PF patients demonstrated that the combination therapy of the anti-senescence drugs dasatinib and quercetin improved physical functional indicators. Given the global aging population and the role of cellular senescence in tissue and organ aging, understanding the impact of cellular senescence on PF is of growing interest. This article systematically summarizes the causes and signaling pathways of cellular senescence in PF. It also objectively analyzes the impact of senescence in AECs and fibroblasts on PF development. Furthermore, potential intervention methods targeting cellular senescence in PF treatment are discussed. This review not only provides a strong theoretical foundation for understanding and manipulating cellular senescence, developing new therapies to improve age-related diseases, and extending a healthy lifespan but also offers hope for reversing the toxicity caused by the massive accumulation of senescence cells in humans.

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References
1.
Shi M, Zhu J, Wang R, Chen X, Mi L, Walz T . Latent TGF-β structure and activation. Nature. 2011; 474(7351):343-9. PMC: 4717672. DOI: 10.1038/nature10152. View

2.
Huang C, Xue X, Gong N, Jiang J . Ginsenoside Rg1 suppresses paraquat-induced epithelial cell senescence by enhancing autophagy in an ATG12-dependent manner. Environ Toxicol. 2022; 37(9):2302-2313. DOI: 10.1002/tox.23597. View

3.
Rayess H, Wang M, Srivatsan E . Cellular senescence and tumor suppressor gene p16. Int J Cancer. 2011; 130(8):1715-25. PMC: 3288293. DOI: 10.1002/ijc.27316. View

4.
Young L, Gulleman P, Short C, Tanjore H, Sherrill T, Qi A . Epithelial-macrophage interactions determine pulmonary fibrosis susceptibility in Hermansky-Pudlak syndrome. JCI Insight. 2016; 1(17):e88947. PMC: 5070955. DOI: 10.1172/jci.insight.88947. View

5.
Bilgili H, Bialas A, Gorski P, Piotrowski W . Telomere Abnormalities in the Pathobiology of Idiopathic Pulmonary Fibrosis. J Clin Med. 2019; 8(8). PMC: 6723768. DOI: 10.3390/jcm8081232. View