Repository of Research and Investigative Information

Repository of Research and Investigative Information

Ilam University of Medical Sciences

Idiopathic pulmonary fibrosis (IPF) signaling pathways and protective roles of melatonin

(2018) Idiopathic pulmonary fibrosis (IPF) signaling pathways and protective roles of melatonin. Life Sciences. pp. 17-29. ISSN 0024-3205

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Abstract

Idiopathic pulmonary fibrosis (IPF) is characterized by the progressive loss of lung function due to tissue scarring. A variety of pro-inflammatory and pro-fibrogenic factors including interleukin-17A, transforming growth factor beta, Wnt/beta-catenin, vascular endothelial growth factor, platelet- derived growth factor, fibroblast growth factors, endotelin-1, renin angiotensin system and impaired caveolin-1 function are involved in the IPF pathogenesis. Current therapies for IPF have some limitations and this highlights the need for effective therapeutic agents to treat this fatal disease. Melatonin and its metabolites are broad-spectrum antioxidants that not only remove reactive oxygen and nitrogen species by radical scavenging but also up-regulate the expression and activity of endogenous antioxidants. Via these actions, melatonin and its metabolites modulate a variety of molecular pathways in different pathophysiological conditions. Herein, we review the signaling pathways involved in the pathophysiology of IPF and the potentially protective effects of melatonin on these pathways.

Item Type: Article
Keywords: Pulmonary fibrosis Melatonin Caveolin-1 Growth factor Wnt/beta-catenin Endothelin-1 Angiotensin II Inflammation growth-factor-beta human lung fibroblasts breast-cancer cells induced hif-1-alpha inactivation induced oxidative stress focal cerebral-ischemia induced liver fibrosis smooth-muscle-cells tgf-beta in-vitro Research & Experimental Medicine Pharmacology & Pharmacy
Page Range: pp. 17-29
Journal or Publication Title: Life Sciences
Journal Index: ISI
Volume: 201
Identification Number: https://doi.org/10.1016/j.lfs.2018.03.032
ISSN: 0024-3205
Depositing User: مهندس مهدی شریفی
URI: http://eprints.medilam.ac.ir/id/eprint/81

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