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

7 Citations (Scopus)

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
Externally publishedYes

Fingerprint

Idiopathic Pulmonary Fibrosis
Melatonin
Metabolites
Antioxidants
Reactive Nitrogen Species
Catenins
Fibroblast Growth Factors
Platelet-Derived Growth Factor
Scavenging
Angiotensins
Transforming Growth Factors
Renin
Vascular Endothelial Growth Factor A
Reactive Oxygen Species
Renin-Angiotensin System
Tissue
Cicatrix
Up-Regulation
Lung
Therapeutics

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

Idiopathic pulmonary fibrosis (IPF) signaling pathways and protective roles of melatonin. / Hosseinzadeh, Azam; Javad-Moosavi, Seyed Ali; Reiter, Russel J; Hemati, Karim; Ghaznavi, Habib; Mehrzadi, Saeed.

In: Life Sciences, Vol. 201, 15.05.2018, p. 17-29.

Research output: Contribution to journalReview article

Hosseinzadeh, A, Javad-Moosavi, SA, Reiter, RJ, Hemati, K, Ghaznavi, H & Mehrzadi, S 2018, 'Idiopathic pulmonary fibrosis (IPF) signaling pathways and protective roles of melatonin', Life Sciences, vol. 201, pp. 17-29. https://doi.org/10.1016/j.lfs.2018.03.032
Hosseinzadeh, Azam ; Javad-Moosavi, Seyed Ali ; Reiter, Russel J ; Hemati, Karim ; Ghaznavi, Habib ; Mehrzadi, Saeed. / Idiopathic pulmonary fibrosis (IPF) signaling pathways and protective roles of melatonin. In: Life Sciences. 2018 ; Vol. 201. pp. 17-29.
@article{602e712fca894709a5a7af1c9108a0ef,
title = "Idiopathic pulmonary fibrosis (IPF) signaling pathways and protective roles of melatonin",
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.",
keywords = "Angiotensin II, Caveolin‑1, Endothelin‑1, Growth factor, Inflammation, Melatonin, Pulmonary fibrosis, Wnt/β‑catenin",
author = "Azam Hosseinzadeh and Javad-Moosavi, {Seyed Ali} and Reiter, {Russel J} and Karim Hemati and Habib Ghaznavi and Saeed Mehrzadi",
year = "2018",
month = "5",
day = "15",
doi = "10.1016/j.lfs.2018.03.032",
language = "English (US)",
volume = "201",
pages = "17--29",
journal = "Life Sciences",
issn = "0024-3205",
publisher = "Elsevier Inc.",

}

TY - JOUR

T1 - Idiopathic pulmonary fibrosis (IPF) signaling pathways and protective roles of melatonin

AU - Hosseinzadeh, Azam

AU - Javad-Moosavi, Seyed Ali

AU - Reiter, Russel J

AU - Hemati, Karim

AU - Ghaznavi, Habib

AU - Mehrzadi, Saeed

PY - 2018/5/15

Y1 - 2018/5/15

N2 - 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.

AB - 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.

KW - Angiotensin II

KW - Caveolin‑1

KW - Endothelin‑1

KW - Growth factor

KW - Inflammation

KW - Melatonin

KW - Pulmonary fibrosis

KW - Wnt/β‑catenin

UR - http://www.scopus.com/inward/record.url?scp=85044118975&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85044118975&partnerID=8YFLogxK

U2 - 10.1016/j.lfs.2018.03.032

DO - 10.1016/j.lfs.2018.03.032

M3 - Review article

VL - 201

SP - 17

EP - 29

JO - Life Sciences

JF - Life Sciences

SN - 0024-3205

ER -