Targeting Growth Factor and Cytokine Pathways to Treat Idiopathic Pulmonary Fibrosis

Idiopathic pulmonary fibrosis (IPF) is a chronic interstitial lung disease of unknown origin that usually results in death from secondary respiratory failure within 2–5 years of diagnosis. Recent studies have identified key roles of cytokine and growth factor pathways in the pathogenesis of IPF. Alt...

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Published inFrontiers in pharmacology Vol. 13; p. 918771
Main Authors Ma, Hongbo, Liu, Shengming, Li, Shanrui, Xia, Yong
Format Journal Article
LanguageEnglish
Published Frontiers Media S.A 03.06.2022
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Summary:Idiopathic pulmonary fibrosis (IPF) is a chronic interstitial lung disease of unknown origin that usually results in death from secondary respiratory failure within 2–5 years of diagnosis. Recent studies have identified key roles of cytokine and growth factor pathways in the pathogenesis of IPF. Although there have been numerous clinical trials of drugs investigating their efficacy in the treatment of IPF, only Pirfenidone and Nintedanib have been approved by the FDA. However, they have some major limitations, such as insufficient efficacy, undesired side effects and poor pharmacokinetic properties. To give more insights into the discovery of potential targets for the treatment of IPF, this review provides an overview of cytokines, growth factors and their signaling pathways in IPF, which have important implications for fully exploiting the therapeutic potential of targeting cytokine and growth factor pathways. Advances in the field of cytokine and growth factor pathways will help slow disease progression, prolong life, and improve the quality of life for IPF patients in the future.
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Riccardo Pozzan, University of Trieste, Italy
Reviewed by: Chiara Bozzi, Ospedale di Cattinara, Italy
Edited by: Barbara Ruaro, University of Trieste, Italy
These authors have contributed equally to this work and share first authorship
This article was submitted to Respiratory Pharmacology, a section of the journal Frontiers in Pharmacology
ISSN:1663-9812
1663-9812
DOI:10.3389/fphar.2022.918771