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Advances in Lung Injury, Regeneration, and Fibrosis 2.0
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Advances in Lung Injury, Regeneration, and Fibrosis 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 June 2024) | Viewed by 437

Special Issue Editor

Prof. Dr. Satish K. Madala

E-Mail Website
Guest Editor
Department of Internal Medicine, Division of Pulmonary, Critical Care, and Sleep Medicine, The University of Cincinnati, Cincinnati, OH 45229, USA
Interests: Idiopathic pulmonary fibrosis; scleroderma; cystic fibrosis; lung injury; allergic asthma
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issue “Advances in Lung Injury, Regeneration, and Fibrosis”. Pulmonary fibrosis, characterized by a progressive loss of lung function, impaired gas exchange, and high mortality, is a pathological endpoint of many pediatric and adult chronic lung diseases. Idiopathic pulmonary fibrosis (IPF) and several autoimmune diseases, including rheumatoid arthritis and systemic sclerosis, are the most commonly occurring types. The molecular mechanisms underlying the early fibrotic response to acute injury and the dysfunctional regeneration in response to chronic injury are poorly understood. In general, the injury response is known to be triggered in part by dysregulated signaling networks within multiple lung cell types, including those of epithelial cells, endothelial, fibroblast, and immune origin. In addition, the disruption of paracrine communication networks between lung cells and their respective extracellular matrix (ECM) proteins further sustains fibrosis and, in severe cases, results in organ destruction. This Special Issue focuses on recent advances in the mechanistic understanding of the dysregulated molecular pathways and cellular networks involved in fibrogenesis. Authors are encouraged to submit both original research articles and reviews on all aspects of the molecular mechanisms underlying lung injury, regeneration, and the progression of pulmonary fibrosis. All submitted articles will undergo peer review.

Prof. Dr. Satish K. Madala
Guest Editor

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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • idiopathic pulmonary fibrosis
  • myofibroblast
  • extracellular matrix
  • infections
  • acute respiratory distress syndrome

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Published Papers (1 paper)

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13 pages, 2428 KiB  
Perspective
The Role of the Extracellular Matrix in the Pathogenesis and Treatment of Pulmonary Emphysema
by Jerome Cantor
Int. J. Mol. Sci. 2024, 25(19), 10613; https://doi.org/10.3390/ijms251910613 - 2 Oct 2024
Viewed by 220
Abstract
Pulmonary emphysema involves progressive destruction of alveolar walls, leading to enlarged air spaces and impaired gas exchange. While the precise mechanisms responsible for these changes remain unclear, there is growing evidence that the extracellular matrix plays a critical role in the process. An [...] Read more.
Pulmonary emphysema involves progressive destruction of alveolar walls, leading to enlarged air spaces and impaired gas exchange. While the precise mechanisms responsible for these changes remain unclear, there is growing evidence that the extracellular matrix plays a critical role in the process. An essential feature of pulmonary emphysema is damage to the elastic fiber network surrounding the airspaces, which stores the energy needed to expel air from the lungs. The degradation of these fibers disrupts the mechanical forces involved in respiration, resulting in distension and rupture of alveolar walls. While the initial repair process mainly consists of elastin degradation and resynthesis, continued alveolar wall injury may be associated with increased collagen deposition, resulting in a mixed pattern of emphysema and interstitial fibrosis. Due to the critical role of elastic fiber injury in pulmonary emphysema, preventing damage to this matrix component has emerged as a potential therapeutic strategy. One treatment approach involves the intratracheal administration of hyaluronan, a polysaccharide that prevents elastin breakdown by binding to lung elastic fibers. In clinical trials, inhalation of aerosolized HA decreased elastic fiber injury, as measured by the release of the elastin-specific cross-linking amino acids, desmosine, and isodesmosine. By protecting elastic fibers from enzymatic and oxidative damage, aerosolized HA could alter the natural history of pulmonary emphysema, thereby reducing the risk of respiratory failure. Full article
(This article belongs to the Special Issue Advances in Lung Injury, Regeneration, and Fibrosis 2.0)
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