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

Azam Hosseinzadeh, Seyed Ali Javad-Moosavi, Russel J. Reiter, Karim Hemati, Habib Ghaznavi, Saeed Mehrzadi

Research output: Contribution to journalReview article

14 Scopus citations

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 β, Wnt/β‑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.

Original languageEnglish (US)
Pages (from-to)17-29
Number of pages13
JournalLife Sciences
Volume201
DOIs
StatePublished - May 15 2018

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Keywords

  • Angiotensin II
  • Caveolin‑1
  • Endothelin‑1
  • Growth factor
  • Inflammation
  • Melatonin
  • Pulmonary fibrosis
  • Wnt/β‑catenin

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

Hosseinzadeh, A., Javad-Moosavi, S. A., Reiter, R. J., Hemati, K., Ghaznavi, H., & Mehrzadi, S. (2018). Idiopathic pulmonary fibrosis (IPF) signaling pathways and protective roles of melatonin. Life Sciences, 201, 17-29. https://doi.org/10.1016/j.lfs.2018.03.032