Oxidative/nitrosative stress, autophagy and apoptosis as therapeutic targets of melatonin in idiopathic pulmonary fibrosis

Azam Hosseinzadeh, Seyed Ali Javad-Moosavi, Russel J Reiter, Rasoul Yarahmadi, Habib Ghaznavi, Saeed Mehrzadi

Research output: Contribution to journalArticle

2 Citations (Scopus)

Abstract

INTRODUCTION: Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease associated with disruption of alveolar epithelial cell layer and expansion of fibroblasts/myofibroblasts. Excessive levels of oxidative/nitrosative stress, induction of apoptosis, and insufficient autophagy may be involved in IPF pathogenesis; hence, the targeting of these pathways may ameliorate IPF. Areas covered: We describe the ameliorative effect of melatonin on IPF. We summarize the research on IPF pathogenesis with a focus on oxidative/nitrosative stress, autophagy and apoptosis pathways and discuss the potential effects of melatonin on these pathways. Expert opinion: Oxidative/nitrosative stress, apoptosis and autophagy could be interesting targets for therapeutic intervention in IPF. Melatonin, as a potent antioxidant, induces the expression of antioxidant enzymes, scavenges free radicals and modulates apoptosis and autophagy pathways. The effect of melatonin in the induction of autophagy could be an important mechanism against fibrotic process in IPF lungs. Further clinical studies are necessary to determine if melatonin could be a candidate for treating IPF.

Original languageEnglish (US)
Pages (from-to)1049-1061
Number of pages13
JournalExpert Opinion on Therapeutic Targets
Volume22
Issue number12
DOIs
StatePublished - Dec 1 2018
Externally publishedYes

Fingerprint

Idiopathic Pulmonary Fibrosis
Oxidative stress
Autophagy
Melatonin
Oxidative Stress
Apoptosis
Antioxidants
Therapeutics
Pulmonary diseases
Fibroblasts
Free Radicals
Alveolar Epithelial Cells
Myofibroblasts
Interstitial Lung Diseases
Expert Testimony
Enzymes
Lung

Keywords

  • apoptosis
  • autophagy
  • melatonin
  • oxidative stress
  • Pulmonary fibrosis

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology
  • Drug Discovery
  • Clinical Biochemistry

Cite this

Oxidative/nitrosative stress, autophagy and apoptosis as therapeutic targets of melatonin in idiopathic pulmonary fibrosis. / Hosseinzadeh, Azam; Javad-Moosavi, Seyed Ali; Reiter, Russel J; Yarahmadi, Rasoul; Ghaznavi, Habib; Mehrzadi, Saeed.

In: Expert Opinion on Therapeutic Targets, Vol. 22, No. 12, 01.12.2018, p. 1049-1061.

Research output: Contribution to journalArticle

Hosseinzadeh, Azam ; Javad-Moosavi, Seyed Ali ; Reiter, Russel J ; Yarahmadi, Rasoul ; Ghaznavi, Habib ; Mehrzadi, Saeed. / Oxidative/nitrosative stress, autophagy and apoptosis as therapeutic targets of melatonin in idiopathic pulmonary fibrosis. In: Expert Opinion on Therapeutic Targets. 2018 ; Vol. 22, No. 12. pp. 1049-1061.
@article{bc4b38876ad9401fa6c21e03a0d074a1,
title = "Oxidative/nitrosative stress, autophagy and apoptosis as therapeutic targets of melatonin in idiopathic pulmonary fibrosis",
abstract = "INTRODUCTION: Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease associated with disruption of alveolar epithelial cell layer and expansion of fibroblasts/myofibroblasts. Excessive levels of oxidative/nitrosative stress, induction of apoptosis, and insufficient autophagy may be involved in IPF pathogenesis; hence, the targeting of these pathways may ameliorate IPF. Areas covered: We describe the ameliorative effect of melatonin on IPF. We summarize the research on IPF pathogenesis with a focus on oxidative/nitrosative stress, autophagy and apoptosis pathways and discuss the potential effects of melatonin on these pathways. Expert opinion: Oxidative/nitrosative stress, apoptosis and autophagy could be interesting targets for therapeutic intervention in IPF. Melatonin, as a potent antioxidant, induces the expression of antioxidant enzymes, scavenges free radicals and modulates apoptosis and autophagy pathways. The effect of melatonin in the induction of autophagy could be an important mechanism against fibrotic process in IPF lungs. Further clinical studies are necessary to determine if melatonin could be a candidate for treating IPF.",
keywords = "apoptosis, autophagy, melatonin, oxidative stress, Pulmonary fibrosis",
author = "Azam Hosseinzadeh and Javad-Moosavi, {Seyed Ali} and Reiter, {Russel J} and Rasoul Yarahmadi and Habib Ghaznavi and Saeed Mehrzadi",
year = "2018",
month = "12",
day = "1",
doi = "10.1080/14728222.2018.1541318",
language = "English (US)",
volume = "22",
pages = "1049--1061",
journal = "Expert Opinion on Therapeutic Targets",
issn = "1472-8222",
publisher = "Informa Healthcare",
number = "12",

}

TY - JOUR

T1 - Oxidative/nitrosative stress, autophagy and apoptosis as therapeutic targets of melatonin in idiopathic pulmonary fibrosis

AU - Hosseinzadeh, Azam

AU - Javad-Moosavi, Seyed Ali

AU - Reiter, Russel J

AU - Yarahmadi, Rasoul

AU - Ghaznavi, Habib

AU - Mehrzadi, Saeed

PY - 2018/12/1

Y1 - 2018/12/1

N2 - INTRODUCTION: Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease associated with disruption of alveolar epithelial cell layer and expansion of fibroblasts/myofibroblasts. Excessive levels of oxidative/nitrosative stress, induction of apoptosis, and insufficient autophagy may be involved in IPF pathogenesis; hence, the targeting of these pathways may ameliorate IPF. Areas covered: We describe the ameliorative effect of melatonin on IPF. We summarize the research on IPF pathogenesis with a focus on oxidative/nitrosative stress, autophagy and apoptosis pathways and discuss the potential effects of melatonin on these pathways. Expert opinion: Oxidative/nitrosative stress, apoptosis and autophagy could be interesting targets for therapeutic intervention in IPF. Melatonin, as a potent antioxidant, induces the expression of antioxidant enzymes, scavenges free radicals and modulates apoptosis and autophagy pathways. The effect of melatonin in the induction of autophagy could be an important mechanism against fibrotic process in IPF lungs. Further clinical studies are necessary to determine if melatonin could be a candidate for treating IPF.

AB - INTRODUCTION: Idiopathic pulmonary fibrosis (IPF) is a fatal interstitial lung disease associated with disruption of alveolar epithelial cell layer and expansion of fibroblasts/myofibroblasts. Excessive levels of oxidative/nitrosative stress, induction of apoptosis, and insufficient autophagy may be involved in IPF pathogenesis; hence, the targeting of these pathways may ameliorate IPF. Areas covered: We describe the ameliorative effect of melatonin on IPF. We summarize the research on IPF pathogenesis with a focus on oxidative/nitrosative stress, autophagy and apoptosis pathways and discuss the potential effects of melatonin on these pathways. Expert opinion: Oxidative/nitrosative stress, apoptosis and autophagy could be interesting targets for therapeutic intervention in IPF. Melatonin, as a potent antioxidant, induces the expression of antioxidant enzymes, scavenges free radicals and modulates apoptosis and autophagy pathways. The effect of melatonin in the induction of autophagy could be an important mechanism against fibrotic process in IPF lungs. Further clinical studies are necessary to determine if melatonin could be a candidate for treating IPF.

KW - apoptosis

KW - autophagy

KW - melatonin

KW - oxidative stress

KW - Pulmonary fibrosis

UR - http://www.scopus.com/inward/record.url?scp=85056734160&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85056734160&partnerID=8YFLogxK

U2 - 10.1080/14728222.2018.1541318

DO - 10.1080/14728222.2018.1541318

M3 - Article

VL - 22

SP - 1049

EP - 1061

JO - Expert Opinion on Therapeutic Targets

JF - Expert Opinion on Therapeutic Targets

SN - 1472-8222

IS - 12

ER -