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  Epigenetic Mechanisms in Parenchymal Lung Diseases: Bystanders or Therapeutic Targets?

Avci, E., Sarvari, P., Savai, R., Seeger, W., & Pullamsetti, S. S. (2022). Epigenetic Mechanisms in Parenchymal Lung Diseases: Bystanders or Therapeutic Targets? INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 23(1): 546. doi:10.3390/ijms23010546.

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 Creators:
Avci, Edibe1, Author              
Sarvari, Pouya1, Author              
Savai, Rajkumar1, Author              
Seeger, Werner1, Author              
Pullamsetti, Soni S.1, Author              
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1Lung Development and Remodeling, Max Planck Institute for Heart and Lung Research, Max Planck Society, ou_2591698              

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 Abstract: Epigenetic responses due to environmental changes alter chromatin structure, which in turn modifies the phenotype, gene expression profile, and activity of each cell type that has a role in the pathophysiology of a disease. Pulmonary diseases are one of the major causes of death in the world, including lung cancer, idiopathic pulmonary fibrosis (IPF), chronic obstructive pulmonary disease (COPD), pulmonary hypertension (PH), lung tuberculosis, pulmonary embolism, and asthma. Several lines of evidence indicate that epigenetic modifications may be one of the main factors to explain the increasing incidence and prevalence of lung diseases including IPF and COPD. Interestingly, isolated fibroblasts and smooth muscle cells from patients with pulmonary diseases such as IPF and PH that were cultured ex vivo maintained the disease phenotype. The cells often show a hyper-proliferative, apoptosis-resistant phenotype with increased expression of extracellular matrix (ECM) and activated focal adhesions suggesting the presence of an epigenetically imprinted phenotype. Moreover, many abnormalities observed in molecular processes in IPF patients are shown to be epigenetically regulated, such as innate immunity, cellular senescence, and apoptotic cell death. DNA methylation, histone modification, and microRNA regulation constitute the most common epigenetic modification mechanisms.

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 Dates: 2022-01-04
 Publication Status: Published online
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 Identifiers: ISI: 000741767000001
DOI: 10.3390/ijms23010546
PMID: 35008971
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Title: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Source Genre: Journal
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Pages: - Volume / Issue: 23 (1) Sequence Number: 546 Start / End Page: - Identifier: -