Next Article in Journal
Letrozole Accelerates Metabolic Remodeling through Activation of Glycolysis in Cardiomyocytes: A Role beyond Hormone Regulation
Next Article in Special Issue
CpG Island Methylator Phenotype—A Hope for the Future or a Road to Nowhere?
Previous Article in Journal
Psoriasis-Associated Inflammatory Conditions Induce IL-23 mRNA Expression in Normal Human Epidermal Keratinocytes
Previous Article in Special Issue
The Regulation of Collagen Processing by miRNAs in Disease and Possible Implications for Bone Turnover
Review

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

1
Department of Lung Development and Remodeling, Max-Planck Institute for Heart and Lung Research, Parkstrasse 1, 61231 Bad Nauheim, Germany
2
Department of Internal Medicine, Justus Liebig University, 35392 Giessen, Germany
3
Institute for Lung Health (ILH), Justus Liebig University, 35392 Giessen, Germany
*
Author to whom correspondence should be addressed.
Academic Editors: Maria M. Sasiadek and Stefanie Krick
Int. J. Mol. Sci. 2022, 23(1), 546; https://doi.org/10.3390/ijms23010546
Received: 2 December 2021 / Revised: 28 December 2021 / Accepted: 30 December 2021 / Published: 4 January 2022
(This article belongs to the Special Issue Epigenetic Mechanisms and Human Pathology 2.0)
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. View Full-Text
Keywords: IPF; COPD; DNA methylation; histone modifications; microRNA; epigenetic editing; gene transfer IPF; COPD; DNA methylation; histone modifications; microRNA; epigenetic editing; gene transfer
Show Figures

Figure 1

MDPI and ACS Style

Avci, E.; Sarvari, P.; Savai, R.; Seeger, W.; Pullamsetti, S.S. Epigenetic Mechanisms in Parenchymal Lung Diseases: Bystanders or Therapeutic Targets? Int. J. Mol. Sci. 2022, 23, 546. https://doi.org/10.3390/ijms23010546

AMA Style

Avci E, Sarvari P, Savai R, Seeger W, Pullamsetti SS. Epigenetic Mechanisms in Parenchymal Lung Diseases: Bystanders or Therapeutic Targets? International Journal of Molecular Sciences. 2022; 23(1):546. https://doi.org/10.3390/ijms23010546

Chicago/Turabian Style

Avci, Edibe, Pouya Sarvari, Rajkumar Savai, Werner Seeger, and Soni S. Pullamsetti. 2022. "Epigenetic Mechanisms in Parenchymal Lung Diseases: Bystanders or Therapeutic Targets?" International Journal of Molecular Sciences 23, no. 1: 546. https://doi.org/10.3390/ijms23010546

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Back to TopTop