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Oxidative/nitrosative stress, autophagy and apoptosis as therapeutic targets of melatonin in idiopathic pulmonary fibrosis.
Expert Opin Ther Targets. 2018 12; 22(12):1049-1061.EO

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.

Authors+Show Affiliations

a Razi Drug Research Center , Iran University of Medical Sciences , Tehran , Iran.b Air Pollution Research Center , Iran University of Medical Sciences , Tehran , Iran.c Department of Cellular and Structural Biology , UT Health , San Antonio , TX , USA.d Department of Occupational Health , Air Pollution Research Center, Iran University of Medical Sciences , Tehran , Iran.e Department of Pharmacology , School of Medicine, Zahedan University of Medical Sciences , Zahedan , Iran.a Razi Drug Research Center , Iran University of Medical Sciences , Tehran , Iran.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

30445883

Citation

Hosseinzadeh, Azam, et al. "Oxidative/nitrosative Stress, Autophagy and Apoptosis as Therapeutic Targets of Melatonin in Idiopathic Pulmonary Fibrosis." Expert Opinion On Therapeutic Targets, vol. 22, no. 12, 2018, pp. 1049-1061.
Hosseinzadeh A, Javad-Moosavi SA, Reiter RJ, et al. Oxidative/nitrosative stress, autophagy and apoptosis as therapeutic targets of melatonin in idiopathic pulmonary fibrosis. Expert Opin Ther Targets. 2018;22(12):1049-1061.
Hosseinzadeh, A., Javad-Moosavi, S. A., Reiter, R. J., Yarahmadi, R., Ghaznavi, H., & Mehrzadi, S. (2018). Oxidative/nitrosative stress, autophagy and apoptosis as therapeutic targets of melatonin in idiopathic pulmonary fibrosis. Expert Opinion On Therapeutic Targets, 22(12), 1049-1061. https://doi.org/10.1080/14728222.2018.1541318
Hosseinzadeh A, et al. Oxidative/nitrosative Stress, Autophagy and Apoptosis as Therapeutic Targets of Melatonin in Idiopathic Pulmonary Fibrosis. Expert Opin Ther Targets. 2018;22(12):1049-1061. PubMed PMID: 30445883.
* Article titles in AMA citation format should be in sentence-case
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, Y1 - 2018/11/16/ PY - 2018/11/18/pubmed PY - 2019/4/18/medline PY - 2018/11/18/entrez KW - Pulmonary fibrosis KW - apoptosis KW - autophagy KW - melatonin KW - oxidative stress SP - 1049 EP - 1061 JF - Expert opinion on therapeutic targets JO - Expert Opin. Ther. Targets VL - 22 IS - 12 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. SN - 1744-7631 UR - https://www.unboundmedicine.com/medline/citation/30445883/Oxidative/nitrosative_stress_autophagy_and_apoptosis_as_therapeutic_targets_of_melatonin_in_idiopathic_pulmonary_fibrosis_ L2 - http://www.tandfonline.com/doi/full/10.1080/14728222.2018.1541318 DB - PRIME DP - Unbound Medicine ER -