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Molecular Advances and Perspectives of Lung Disease: 2nd Edition

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: 30 April 2025 | Viewed by 1314

Special Issue Editor


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Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issue, “Molecular Advances and Perspectives of Lung Disease”. Lung disease is characterized as lung tissue disorder and respiratory dysfunction, including asthma, chronic obstructive pulmonary disease (COPD), pneumonia and tuberculosis, lung cancer, pulmonary hypertension, pulmonary fibrosis, and many other respiratory diseases. Lung disease is a common disease and affects more than tens of millions of people in the U.S. Infection, smoking, pollution, and gene mutations cause most lung diseases, while the potential mechanisms of various lung diseases are still elusive. Due to limited effective pharmaceutic and therapeutic approaches, millions of people continue to struggle with lung disease and suffer from breathing problems. Therefore, understanding the molecular mechanism of lung disease and developing novel pharmaceutical and therapeutic approaches to respiratory disease are urgently needed. This Special Issue plans to give an overview of the most recent advances in the field of molecular mechanisms and pharmacological progression for lung disease.

This Special Issue is aimed at providing selected contributions on advances in the molecular mechanism of lung disease. Potential topics include, but are not limited to:

  • Molecular mechanism of lung disease;
  • Novel therapeutic approaches to lung disease;
  • New model for lung disease;
  • Innate immunity in lung disease;
  • Novel drug deliverry approaches for lung disease;
  • Drug discovery for lung disease.

Dr. Longshuang Huang
Guest Editor

Manuscript Submission Information

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Keywords

  • lung disease
  • inflammation
  • regeneration
  • infection
  • drug discovery

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Published Papers (2 papers)

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Research

24 pages, 9049 KiB  
Article
Assessment of Methylation in Selected ADAMTS Family Genes in Non-Small-Cell Lung Cancer
by Dagmara Szmajda-Krygier, Zuzanna Nocoń, Jacek Pietrzak, Adrian Krygier and Ewa Balcerczak
Int. J. Mol. Sci. 2025, 26(3), 934; https://doi.org/10.3390/ijms26030934 - 23 Jan 2025
Viewed by 481
Abstract
Alterations in the methylation of genetic material can influence carcinogenesis by the downregulation or overexpression of ADAMTS (a disintegrin-like and metalloprotease with thrombospondin motifs) protease genes. Through their proteolytic activity, these enzymes are also capable of promoting angiogenesis. Consequently, ADAMTS proteases can either [...] Read more.
Alterations in the methylation of genetic material can influence carcinogenesis by the downregulation or overexpression of ADAMTS (a disintegrin-like and metalloprotease with thrombospondin motifs) protease genes. Through their proteolytic activity, these enzymes are also capable of promoting angiogenesis. Consequently, ADAMTS proteases can either facilitate or inhibit cancer progression. This study aimed to evaluate the methylation levels of the ADAMTS6, ADAMTS9, and ADAMTS12 genes in non-small-cell lung cancer (NSCLC) using data from bioinformatics databases. The focus was on differences between lung adenocarcinoma (LUAD) and lung squamous-cell carcinoma (LUSC) subtypes and their impact on patient overall survival (OS). ADAMTS6 gene expression is significantly reduced in LUSC, and analysis of ADAMTS9 gene expression showed a significantly reduced gene transcript level in LUAD and LUSC, while both NSCLC subtypes demonstrated ADAMTS12 upregulation. In LUSC, significantly elevated promoter methylation was found in all of the aforementioned genes, while in LUAD, higher promoter methylation was observed only for ADAMTS9 and ADAMTS12. The differential methylation region (DMR) pattern demonstrated by ADAMTS6, ADAMTS9, and ADAMTS12 is a useful tool for distinguishing normal from cancer cells. The areas under the curve (AUCs) ranged from 0.86 to 0.99 for both LUAD and LUSC subtypes. The methylation level of different CpG sites among selected ADAMTS members is related to patient survival, suggesting it may have value as a prognostic marker. The methylation degree of promoter regions in genes encoding ADAMTS family proteins could significantly influence LUSC and LUAD. Increased promoter methylation could also reduce certain gene expression, contributing to cancer progression. The expression levels and specific DMRs of ADAMTS genes may serve as prognostic markers correlating with patient OS. Assessing ADAMTS gene methylation could become a diagnostic tool for differentiating NSCLC subtypes and potentially guide therapeutic strategies. Further research is needed to fully understand the activity and mechanisms of ADAMTS family proteins. Full article
(This article belongs to the Special Issue Molecular Advances and Perspectives of Lung Disease: 2nd Edition)
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12 pages, 368 KiB  
Communication
Evaluation of Polygenic Risk Score for Prediction of Childhood Onset and Severity of Asthma
by Olga Savelieva, Alexandra Karunas, Inga Prokopenko, Zhanna Balkhiyarova, Irina Gilyazova, Irina Khidiyatova and Elza Khusnutdinova
Int. J. Mol. Sci. 2025, 26(1), 103; https://doi.org/10.3390/ijms26010103 - 26 Dec 2024
Viewed by 616
Abstract
Asthma is a common complex disease with susceptibility defined through an interplay of genetic and environmental factors. Responsiveness to asthma treatment varies between individuals and is largely determined by genetic variability. The polygenic score (PGS) approach enables an individual risk of asthma and [...] Read more.
Asthma is a common complex disease with susceptibility defined through an interplay of genetic and environmental factors. Responsiveness to asthma treatment varies between individuals and is largely determined by genetic variability. The polygenic score (PGS) approach enables an individual risk of asthma and respective response to drug therapy. PGS models could help to predict the individual risk of asthma using 26 SNPs of drug pathway genes involved in the metabolism of glucocorticosteroids (GCS), and beta-2-agonists, antihistamines, and antileukotriene drugs associated with the response to asthma treatment within GWAS were built. For PGS, summary statistics from the Trans-National Asthma Genetic Consortium GWAS meta-analysis, and genotype data for 882 individuals with asthma/controls from the Volga-Ural region, were used. The study group was comprised of Russian, Tatar, Bashkir, and mixed ethnicity individuals with asthma (N = 378) aged 2–18 years. and individuals without features of atopic disease (N = 504) aged 4–67 years from the Volga-Ural region. The DNA samples for the study were collected from 2000 to 2021. The drug pathway genes’ PGS revealed a higher odds for childhood asthma risk (p = 2.41 × 10−12). The receiver operating characteristic (ROC) analysis showed an Area Under the Curve, AUC = 0.63. The AUC of average significance for moderate-to-severe and severe asthma was observed (p = 5.7 × 10−9, AUC = 0.64). Asthma drug response pathway gene variant PGS models may contribute to the development of modern approaches to optimise asthma diagnostics and treatment. Full article
(This article belongs to the Special Issue Molecular Advances and Perspectives of Lung Disease: 2nd Edition)
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