Recent Advances in Epithelial Cells in Human Lung Disease

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 2392

Special Issue Editors


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Guest Editor
Department of Medicine, Royal College of Surgeons in Ireland, Dublin, Ireland
Interests: cystic fibrosis; microRNA; induced pluripotent stem cell derived 3D organoid models; airway epithelial cell biology; Innate Immunity

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Guest Editor
School of Pharmacy and Biomolecular Sciences, Royal College of Surgeons in Ireland, Dublin, Ireland
Interests: circRNA; cystic fibrosis; pulmonary fibrosis; COVID-19; epigenetics

Special Issue Information

Dear Colleagues,

Diverse cells of the airway epithelium play critical roles in response to injury, host defense, and the maintenance of homeostasis in the lung. When compromised, they also significantly contribute to human lung disease. Advances in cell biology over the last decade have yielded human in vitro research platforms derived from airway cells, and the epigenetic profiling of these models has the potential to discover key factors that regulate gene expression alterations in lung disease.

For example, human 3D organoid platforms have been demonstrated to be amenable to gene editing and personalized disease modelling, and transcriptomic analysis using single-cell RNA sequencing (scRNA-seq) has revealed substantial airway cell heterogeneity and uncovered previously unknown cell populations. Characterizing the role and function of existing and newly discovered epithelial cell populations is essential in order to provide clues to disease pathogenesis and treatment discovery.

This Special Issue aims to expand our understanding of complex molecular pathways within the airway epithelium in the pathophysiology of pulmonary diseases such as cystic fibrosis, pulmonary fibrosis, chronic obstructive pulmonary disease, and COVID-19 using personalized disease models and omics technology, as well as explore insights into novel therapeutics and drug delivery strategies.

Dr. Irene Oglesby
Dr. Chiara De Santi
Guest Editors

Manuscript Submission Information

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • pulmonary disease
  • personalised disease modelling
  • epithelial cells
  • induced pluripotent stem cells
  • transcriptomics
  • epigenetics
  • scRNA-seq

Published Papers (1 paper)

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Review

14 pages, 1110 KiB  
Review
Airway Epithelium Senescence as a Driving Mechanism in COPD Pathogenesis
by Georgia Bateman, Hong Guo-Parke, Aoife M. Rodgers, Dermot Linden, Melanie Bailey, Sinéad Weldon, Joseph C. Kidney and Clifford C. Taggart
Biomedicines 2023, 11(7), 2072; https://doi.org/10.3390/biomedicines11072072 - 23 Jul 2023
Cited by 2 | Viewed by 1948
Abstract
Cellular senescence is a state of permanent cell cycle arrest triggered by various intrinsic and extrinsic stressors. Cellular senescence results in impaired tissue repair and remodeling, loss of physiological integrity, organ dysfunction, and changes in the secretome. The systemic accumulation of senescence cells [...] Read more.
Cellular senescence is a state of permanent cell cycle arrest triggered by various intrinsic and extrinsic stressors. Cellular senescence results in impaired tissue repair and remodeling, loss of physiological integrity, organ dysfunction, and changes in the secretome. The systemic accumulation of senescence cells has been observed in many age-related diseases. Likewise, cellular senescence has been implicated as a risk factor and driving mechanism in chronic obstructive pulmonary disease (COPD) pathogenesis. Airway epithelium exhibits hallmark features of senescence in COPD including activation of the p53/p21WAF1/CIP1 and p16INK4A/RB pathways, leading to cell cycle arrest. Airway epithelial senescent cells secrete an array of inflammatory mediators, the so-called senescence-associated secretory phenotype (SASP), leading to a persistent low-grade chronic inflammation in COPD. SASP further promotes senescence in an autocrine and paracrine manner, potentially contributing to the onset and progression of COPD. In addition, cellular senescence in COPD airway epithelium is associated with telomere dysfunction, DNA damage, and oxidative stress. This review discusses the potential mechanisms of airway epithelial cell senescence in COPD, the impact of cellular senescence on the development and severity of the disease, and highlights potential targets for modulating cellular senescence in airway epithelium as a potential therapeutic approach in COPD. Full article
(This article belongs to the Special Issue Recent Advances in Epithelial Cells in Human Lung Disease)
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