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Biomolecules
Special Issues
Molecular Mechanisms in Lung Injury, Repair, and Remodeling
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Molecular Mechanisms in Lung Injury, Repair, and Remodeling

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (20 November 2022) | Viewed by 12569

Special Issue Editors

Prof. Dr. Yutong Zhao

E-Mail Website
Guest Editor
Department of Physiology and Cell Biology, Ohio State University, Columbus, OH 43210, USA
Interests: lung epithelial barrier integrity; lysophospholipids; pulmonary fibrosis; lung injury
Dr. Megan Ballinger

E-Mail Website
Guest Editor
Department of Internal Medicine, The Ohio State University, Columbus, OH 43210, USA
Interests: macrophage; innate immunity; pulmonary fibrosis; chronic lung disease
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The lungs are at the interface of the body and the external environment and their main role is to allow gas exchange. The exchange of carbon dioxide for oxygen occurs within the alveoli, which contain structural cells, including alveolar epithelial and microvascular endothelial cells, as well as immune cells, such as macrophages. Exposure of the lung to pathogens, environmental pollutants, or allergens can cause damage to the airways and alveoli, thus compromising our ability to breathe. One such condition is, acute respiratory distress syndrome (ARDS), which can be caused by inhaled pathogens including SARS-CoV-2 as well as other bacteria and virus. ARDS is characterized by diffused alveolar damage, cytokine storm, neutrophil infiltration into alveolar spaces, epithelial and endothelial barrier disruption, and edema. In some cases, the injured lungs can be repaired and lung function can be restored; however, in other cases there is excessive lung repair and remodeling may cause lung fibroblast proliferation, differentiation to myofibroblasts, and extracellular matrix remodeling, resulting in lung fibrosis. Understanding the molecular mechanisms of lung injury, repair and remodeling is a critical need in order to development novel therapeutics and treatments. 

In this Special issue of Biomolecules, we invite your contributions, either in the form of original research articles or reviews on all aspects related to molecular mechanisms in lung injury, repair, and remodeling.

Prof. Dr. Yutong Zhao
Dr. Megan Ballinger
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 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

  • lung injury
  • lung repair
  • lung remodeling
  • ARDS
  • lung epithelial barrier integrity
  • pulmonary fibrosis

Published Papers (3 papers)

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Research

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11 pages, 3221 KiB  
Article
Molecular Regulation of Heme Oxygenase-1 Expression by E2F Transcription Factor 2 in Lung Fibroblast Cells: Relevance to Idiopathic Pulmonary Fibrosis
by Qinmao Ye, Sarah J. Taleb, Heather Wang, Narasimham L. Parinandi, Daniel J. Kass, Mauricio Rojas, Cankun Wang, Qin Ma, Jing Zhao and Yutong Zhao
Biomolecules 2022, 12(10), 1531; https://doi.org/10.3390/biom12101531 - 21 Oct 2022
Cited by 3 | Viewed by 1795
Abstract
Idiopathic pulmonary fibrosis (IPF) is a fatal chronic lung disease. Heme oxygenase-1 (HMOX1/HO-1) is an enzyme that catalyzes the degradation of heme. The role of HO-1 in the pathogenesis of IPF has been studied; however, the molecular regulation of HO-1 and its role [...] Read more.
Idiopathic pulmonary fibrosis (IPF) is a fatal chronic lung disease. Heme oxygenase-1 (HMOX1/HO-1) is an enzyme that catalyzes the degradation of heme. The role of HO-1 in the pathogenesis of IPF has been studied; however, the molecular regulation of HO-1 and its role in IPF are still unclear. In this study, we found that HO-1 protein levels significantly increased in lung myofibroblasts in IPF patients and in lungs in a murine model of bleomycin-induced lung fibrosis. In addition, we observed that administration of a E2F transcription factor inhibitor elevated HO-1 mRNA and protein levels in lung fibroblasts. Downregulation of E2F2 by siRNA transfection increased HO-1 mRNA and protein levels, while overexpression of E2F2 reduced HO-1 levels. However, overexpression of E2F2 did not alter hemin-induced HO-1 protein levels. Furthermore, modulation of HO-1 levels regulated TGF-β1-induced myofibroblast differentiation without altering the phosphorylation of Smad2/3 in lung fibroblast cells. Moreover, the phosphorylation of protein kinase B (Akt) was significantly upregulated in HO-1-depleted lung fibroblast cells. In summary, this study demonstrated that E2F2 regulates the baseline expression of HO-1, but has no effect on modulating HO-1 expression by hemin. Finally, elevated HO-1 expression contributes to the TGF-β1-induced lung myofibroblast differentiation through the activation of the serine/threonine kinase AKT pathway. Overall, our findings suggest that targeting E2F2/HO-1 might be a new therapeutic strategy to treat fibrotic diseases such as IPF. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Lung Injury, Repair, and Remodeling)
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Review

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31 pages, 3167 KiB  
Review
Lung Organoids in Smoking Research: Current Advances and Future Promises
by Hina Agraval and Hong Wei Chu
Biomolecules 2022, 12(10), 1463; https://doi.org/10.3390/biom12101463 - 12 Oct 2022
Cited by 3 | Viewed by 4793
Abstract
Tobacco smoking has been established to contribute to the pathogenesis of various respiratory diseases including chronic obstructive pulmonary disease (COPD), lung cancer, and asthma. However, major hurdles in mechanistic studies on the role of smoking in human lungs remain in part due to [...] Read more.
Tobacco smoking has been established to contribute to the pathogenesis of various respiratory diseases including chronic obstructive pulmonary disease (COPD), lung cancer, and asthma. However, major hurdles in mechanistic studies on the role of smoking in human lungs remain in part due to the lack of ex vivo experimental models and ambiguous data from animal models that can best recapitulate the architecture and pathophysiology of the human lung. Recent development of the lung organoid culture system has opened new avenues for respiratory disease research as organoids are proving to be a sophisticated ex vivo model that functionally and structurally mimics the human lungs better than other traditionally used models. This review will discuss how recent advances in lung organoid systems may help us better determine the injurious and immunological effect of smoking on human lungs and will provide some suggestions for future research directions. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Lung Injury, Repair, and Remodeling)
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20 pages, 1470 KiB  
Review
New Insights into the Alveolar Epithelium as a Driver of Acute Respiratory Distress Syndrome
by Marilia Sanches Santos Rizzo Zuttion, Sarah Kathryn Littlehale Moore, Peter Chen, Andrew Kota Beppu and Jaime Lynn Hook
Biomolecules 2022, 12(9), 1273; https://doi.org/10.3390/biom12091273 - 10 Sep 2022
Cited by 8 | Viewed by 5202
Abstract
The alveolar epithelium serves as a barrier between the body and the external environment. To maintain efficient gas exchange, the alveolar epithelium has evolved to withstand and rapidly respond to an assortment of inhaled, injury-inducing stimuli. However, alveolar damage can lead to loss [...] Read more.
The alveolar epithelium serves as a barrier between the body and the external environment. To maintain efficient gas exchange, the alveolar epithelium has evolved to withstand and rapidly respond to an assortment of inhaled, injury-inducing stimuli. However, alveolar damage can lead to loss of alveolar fluid barrier function and exuberant, non-resolving inflammation that manifests clinically as acute respiratory distress syndrome (ARDS). This review discusses recent discoveries related to mechanisms of alveolar homeostasis, injury, repair, and regeneration, with a contemporary emphasis on virus-induced lung injury. In addition, we address new insights into how the alveolar epithelium coordinates injury-induced lung inflammation and review maladaptive lung responses to alveolar damage that drive ARDS and pathologic lung remodeling. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Lung Injury, Repair, and Remodeling)
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