Summary of - Molecular Pathways and Role of Epigenetics in Idiopathic Pulmonary Fibrosis

Document Type

Article

Abstract

Study Background: The review article titled “Molecular pathways and role of epigenetics in idiopathic pulmonary fibrosis” by Dr. Varalakshmi Velagacherla, Dr. Chetan Hasmukh Mehta, Dr. Yogendra Nayak, and Dr. Usha Yogendra Nayak focuses on the intricate molecular mechanisms and epigenetic factors involved in the pathogenesis of idiopathic pulmonary fibrosis (IPF). IPF is a fatal, progressive lung disease characterized by the scarring of lung tissue, which can lead to lung cancer and other serious conditions.

Research Goals and Hypotheses: The primary goal of this review is to provide an in-depth analysis of the various molecular pathways and epigenetic modifications that contribute to the development and progression of IPF. It highlights the role of environmental and genetic factors in IPF pathogenesis and explores potential epigenetic drug targets for therapeutic intervention.

Methodological Approach:

  1. The review examines epigenetic pathways such as nucleosome remodeling, DNA methylation, histone modifications, and miRNA-mediated gene regulation in the context of IPF.
  1. The current review highlights the relevance of these epigenetic pathways and molecular mechanisms in the pathogenesis of IPF, assessing their impact on fibrosis, inflammation, and myofibroblast proliferation.
  1. It also discusses the role of genetic mutations and transcriptional changes due to environmental factors in the progression of IPF.

Results and Discoveries:

  1. Epigenetic Modifications: Epigenetic changes, including DNA methylation and histone modifications, play a crucial role in IPF development by regulating gene expression. Mutations in genes such as human telomerase reverse transcriptase (hTERT) are associated with decreased life expectancy in IPF patients, especially in chronic smokers.
  1. Molecular Pathways: Key molecular pathways involved in IPF include transforming growth factor-beta (TGF-β), tumor necrosis factor-alpha (TNF-α), platelet-derived growth factor (PDGF), and vascular endothelial growth factor (VEGF). These pathways contribute to fibrosis, inflammation, and the proliferation of myofibroblasts.
  1. Therapeutic Interventions: Current drugs like nintedanib and pirfenidone target VEGF and TGF-β, respectively, showing efficacy in managing IPF. Newer drugs, such as Celgene-CC90001 and FibroGen-FG-3019, are under investigation for their ability to modulate epigenetic mechanisms.

Citation to the base paper: A. Wongkarnjana, T. Yanagihara, M.R. Kolb, Treatment of idiopathic pulmonary fibrosis with nintedanib: an update, Expert Rev.Respir. Med. 13 (2019) 1139–1146

Publication Date

2022

Recommended Citation

Velagacherla, V.; Mehta, C.H.; Nayak, Y.; Nayak, U.Y. Molecular Pathways and Role of Epigenetics in the Idiopathic Pulmonary Fibrosis. Life Sci 2022, 291.

Publication Date

2022

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