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Molecular Advances in Lung Diseases 2.0
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Molecular Advances in Lung Diseases 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: 20 January 2025 | Viewed by 5376

Special Issue Editor

Prof. Dr. Judit E. Pongracz

E-Mail Website
Guest Editor
Pharmaceutical Biotechnology, School of Pharmacy, University of Pecs, 2 Rokus Str, H-7624 Pecs, Hungary
Interests: lung cancers; lymphangioleiomyomatosis; metabolic regulation; Wnt signaling; aging; immune system and chemotherapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is the second volume of our previous Special Issue "Molecular Advances in Lung Diseases". Pulmonary pathology includes a wide spectrum of both neoplastic and non-neoplastic diseases. Such pulmonary pathologies are often the result of the unique connection between the lung tissue and the outside world. Every breath brings in the lung infectious and noxious agents, organic and inorganic particles that can affect the lung unfiltered and can cause pathologies. Despite the various defence mechanisms present in the lung, serious diseases still develop. Any damage to the pulmonary tissue system due to inherited genetic diseases, acquired mutation induced neoplastic diseases, infections or ineffective immune mechanisms have a clear molecular basis, even if the scientific and medical community is not always aware of the complex connections. 

Better understanding of diseases affecting both pulmonary morphology and mechanism of diseases is required for the development of better preventive measures, identification of diagnostic markers and novel therapies that are more effective.

To make the leap from the unknown to translation of scientific research of lung diseases, every morsel of new information counts. The present special issue awaits such scientific research articles and complex reviews that describe molecular advances in understanding of lung diseases to expand the opportunity to catalogue, connect and prepare the results for medical translation.

Prof. Dr. Judit E. Pongracz
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.

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Published Papers (3 papers)

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Research

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16 pages, 15682 KiB  
Article
High Stretch Associated with Mechanical Ventilation Promotes Piezo1-Mediated Migration of Airway Smooth Muscle Cells
by Mingzhi Luo, Rong Gu, Chunhong Wang, Jia Guo, Xiangrong Zhang, Kai Ni, Lei Liu, Yan Pan, Jingjing Li and Linhong Deng
Int. J. Mol. Sci. 2024, 25(3), 1748; https://doi.org/10.3390/ijms25031748 - 1 Feb 2024
Cited by 3 | Viewed by 1615
Abstract
Ventilator-induced lung injury (VILI) during mechanical ventilation (MV) has been attributed to airway remodeling involving increased airway smooth muscle cells (ASMCs), but the underlying mechanism is not fully understood. Thus, we aimed to investigate whether MV-associated high stretch (>10% strain) could modulate mechanosensitive [...] Read more.
Ventilator-induced lung injury (VILI) during mechanical ventilation (MV) has been attributed to airway remodeling involving increased airway smooth muscle cells (ASMCs), but the underlying mechanism is not fully understood. Thus, we aimed to investigate whether MV-associated high stretch (>10% strain) could modulate mechanosensitive Piezo1 expression and thereby alter cell migration of ASMCs as a potential pathway to increased ASMCs in VILI. C57BL/6 mice and ASMCs were subjected to MV at high tidal volume (VT, 18 mL/kg, 3 h) and high stretch (13% strain, 0.5 Hz, 72 h), respectively. Subsequently, the mice or cells were evaluated for Piezo1 and integrin mRNA expression by immunohistochemical staining and quantitative PCR (qPCR), and cell migration and adhesion by transwell and cell adhesion assays. Cells were either treated or not with Piezo1 siRNA, Piezo1-eGFP, Piezo1 knockin, Y27632, or blebbistatin to regulate Piezo1 mRNA expression or inhibit Rho-associated kinase (ROCK) signaling prior to migration or adhesion assessment. We found that expression of Piezo1 in in situ lung tissue, mRNA expression of Piezo1 and integrin αVβ1 and cell adhesion of ASMCs isolated from mice with MV were all reduced but the cell migration of primary ASMCs (pASMCs) isolated from mice with MV was greatly enhanced. Similarly, cell line mouse ASMCs (mASMCs) cultured in vitro with high stretch showed that mRNA expression of Piezo1 and integrin αVβ1 and cell adhesion were all reduced but cell migration was greatly enhanced. Interestingly, such effects of MV or high stretch on ASMCs could be either induced or abolished/reversed by down/up-regulation of Piezo1 mRNA expression and inhibition of ROCK signaling. High stretch associated with MV appears to be a mechanical modulator of Piezo1 mRNA expression and can, thus, promote cell migration of ASMCs during therapeutic MV. This may be a novel mechanism of detrimental airway remodeling associated with MV, and, therefore, a potential intervention target to treat VILI. Full article
(This article belongs to the Special Issue Molecular Advances in Lung Diseases 2.0)
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Review

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19 pages, 1883 KiB  
Review
Emerging Nanomedicine Approaches in Targeted Lung Cancer Treatment
by Isaic Alexandru, Lavinia Davidescu, Alexandru Cătălin Motofelea, Tudor Ciocarlie, Nadica Motofelea, Dan Costachescu, Monica Steluta Marc, Noemi Suppini, Alina Simona Șovrea, Răzvan-Lucian Coșeriu, Daniela-Andreea Bondor, Laura-Gabriela Bobeică and Andreea Crintea
Int. J. Mol. Sci. 2024, 25(20), 11235; https://doi.org/10.3390/ijms252011235 - 19 Oct 2024
Viewed by 968
Abstract
Lung cancer, the leading cause of cancer-related deaths worldwide, is characterized by its aggressive nature and poor prognosis. As traditional chemotherapy has the disadvantage of non-specificity, nanomedicine offers innovative approaches for targeted therapy, particularly through the development of nanoparticles that can deliver therapeutic [...] Read more.
Lung cancer, the leading cause of cancer-related deaths worldwide, is characterized by its aggressive nature and poor prognosis. As traditional chemotherapy has the disadvantage of non-specificity, nanomedicine offers innovative approaches for targeted therapy, particularly through the development of nanoparticles that can deliver therapeutic agents directly to cancer cells, minimizing systemic toxicity and enhancing treatment efficacy. VEGF and VEGFR are shown to be responsible for activating different signaling cascades, which will ultimately enhance tumor development, angiogenesis, and metastasis. By inhibiting VEGF and VEGFR signaling pathways, these nanotherapeutics can effectively disrupt tumor angiogenesis and proliferation. This review highlights recent advancements in nanoparticle design, including lipid-based, polymeric, and inorganic nanoparticles, and their clinical implications in improving lung cancer outcomes, exploring the role of nanomedicine in lung cancer diagnoses and treatment. Full article
(This article belongs to the Special Issue Molecular Advances in Lung Diseases 2.0)
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26 pages, 1325 KiB  
Review
The Role of Peptides in Asthma–Obesity Phenotype
by Ewelina Russjan
Int. J. Mol. Sci. 2024, 25(6), 3213; https://doi.org/10.3390/ijms25063213 - 12 Mar 2024
Cited by 2 | Viewed by 2209
Abstract
The co-occurrence of asthma and obesity is becoming an increasingly common health problem. It became clear that both diseases are closely related, since overweight/obesity are associated with an increased risk of asthma development, and more than half of the subjects with severe or [...] Read more.
The co-occurrence of asthma and obesity is becoming an increasingly common health problem. It became clear that both diseases are closely related, since overweight/obesity are associated with an increased risk of asthma development, and more than half of the subjects with severe or difficult-to-treat asthma are obese. Currently, there are no specific guidelines for the treatment of this group of patients. The mechanisms involved in the asthma–obesity phenotype include low-grade chronic inflammation and changes in pulmonary physiology. However, genetic predispositions, gender differences, comorbid conditions, and gut microbiota also seem to be important. Regulatory peptides affect many processes related to the functioning of the respiratory tract and adipose tissue. Adipokines such as leptin, adiponectin, resistin, and the less studied omentin, chemerin, and visfatin, as well as the gastrointestinal hormones ghrelin, cholecystokinin, glucagon-like peptide-1, and neuropeptides, including substance P or neuropeptide Y, can play a significant role in asthma with obesity. The aim of this article is to provide a concise review of the contribution of particular peptides in inflammatory reactions, obesity, asthma, and a combination of both diseases, as well as emphasize their potential role in the effective treatment of the asthma–obesity phenotype in the future. Full article
(This article belongs to the Special Issue Molecular Advances in Lung Diseases 2.0)
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