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Advanced Molecular Research in Lung Diseases
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Advanced Molecular Research in Lung Diseases

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 (20 November 2024) | Viewed by 9345

Special Issue Editor

Dr. Yun-Min Zheng

E-Mail Website
Guest Editor
Department of Molecular and Cellular Physiology, Albany Medical College, Albany, NY 12208, USA
Interests: lung biology and disease; gene expression and regulation; signal transduction; redox signaling
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

The primary functions of the respiratory system are to provide oxygen and nutrients for the cells of the body and to simultaneously expel carbon dioxide and other waste products. Chronic respiratory diseases such as asthma, chronic obstructive pulmonary disease (COPD), pulmonary hypertension, interstitial lung disease, etc., can result in permanent destruction of the airways and structures of the lungs. An estimated 545 million patients suffer from a chronic respiratory disease worldwide, making them leading causes of disability and mortality. Rising prevalence has resulted in extensive health and economic burdens for patients and healthcare systems.

Current treatments in chronic lung diseases may be scarce, or when available are still lacking. They are non-curative and often lack specificity and efficacy. Fortunately, scientific progress in the study of lung diseases has been made in various aspects, ranging from our understanding of cellular processes to the identification of investigative biomarkers for diagnosis and prognosis and the development of new clinical therapies.

This Special Issue seeks to inform readers of cutting-edge molecular mechanisms and therapy in lung health and disease. We invite members of the scientific community to share original manuscripts and complete review articles highlighting their latest findings in this area.

Dr. Yun-Min Zheng
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

  • lung diseases
  • cellular processes
  • molecular mechanisms
  • new drug discoveries
  • novel treatment options

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Published Papers (5 papers)

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Research

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16 pages, 1891 KiB  
Article
Mitochondrial COX3 and tRNA Gene Variants Associated with Risk and Prognosis of Idiopathic Pulmonary Fibrosis
by Li-Na Lee, I-Shiow Jan, Wen-Ru Chou, Wei-Lun Liu, Yen-Liang Kuo, Chih-Yueh Chang, Hsiu-Ching Chang, Jia-Luen Liu, Chia-Lin Hsu, Chia-Nan Lin, Ke-Yun Chao, Chi-Wei Tseng, I-Hsien Lee, Jann-Tay Wang and Jann-Yuan Wang
Int. J. Mol. Sci. 2025, 26(3), 1378; https://doi.org/10.3390/ijms26031378 - 6 Feb 2025
Viewed by 807
Abstract
Idiopathic pulmonary fibrosis (IPF) has been associated with mitochondrial dysfunction. We investigated whether mitochondrial DNA variants in peripheral blood leukocytes (PBLs), which affect proteins of the respiratory chain and mitochondrial function, could be associated with an increased risk and poor prognosis of IPF. [...] Read more.
Idiopathic pulmonary fibrosis (IPF) has been associated with mitochondrial dysfunction. We investigated whether mitochondrial DNA variants in peripheral blood leukocytes (PBLs), which affect proteins of the respiratory chain and mitochondrial function, could be associated with an increased risk and poor prognosis of IPF. From 2020 to 2022, we recruited 36 patients (age: 75.3 ± 8.5; female: 19%) with IPF, and 80 control subjects (age: 72.3 ± 9.0; female: 27%). The mitochondrial genome of peripheral blood leukocytes was determined using next-generation sequencing. During a 45-month follow-up, 10 (28%) patients with IPF remained stable and the other 26 (72%) progressed, with 12 (33%) mortalities. IPF patients had more non-synonymous (NS) variants (substitution/deletion/insertion) in mitochondrial COX3 gene (coding for subunit 3 of complex IV of the respiratory chain), and more mitochondrial tRNA variants located in the anticodon (AC) stem, AC loop, variable loop, T-arm, and T-loop of the tRNA clover-leaf structure in PBLs than the control group. The succumbed IPF patients were older, had lower initial diffusion capacity, and higher initial fibrosis score on high-resolution computerized tomography (HRCT) than the alive group. NS variants in mitochondrial COX3 gene and tRNA variants in PBLs were associated with shorter survival. Our study shows that (1) leukocyte mitochondrial COX3 NS variants are associated with risk and prognosis of IPF; (2) leukocyte mitochondrial tRNA variants located in the AC stem, AC loop, variable loop, T-arm, and T-loop of the tRNA clover-leaf structure are associated with risk, and the presence of tRNA variants is associated with poor prognosis of IPF. Full article
(This article belongs to the Special Issue Advanced Molecular Research in Lung Diseases)
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23 pages, 3620 KiB  
Article
Glycogen Synthase Kinase-3 Inhibition by CHIR99021 Promotes Alveolar Epithelial Cell Proliferation and Lung Regeneration in the Lipopolysaccharide-Induced Acute Lung Injury Mouse Model
by Raquel Fernandes, Catarina Barbosa-Matos, Caroline Borges-Pereira, Ana Luísa Rodrigues Toste de Carvalho and Sandra Costa
Int. J. Mol. Sci. 2024, 25(2), 1279; https://doi.org/10.3390/ijms25021279 - 20 Jan 2024
Cited by 1 | Viewed by 2200
Abstract
Acute respiratory distress syndrome (ARDS) is a life-threatening lung injury that currently lacks effective clinical treatments. Evidence highlights the potential role of glycogen synthase kinase-3 (GSK-3) inhibition in mitigating severe inflammation. The inhibition of GSK-3α/β by CHIR99021 promoted fetal lung progenitor proliferation and [...] Read more.
Acute respiratory distress syndrome (ARDS) is a life-threatening lung injury that currently lacks effective clinical treatments. Evidence highlights the potential role of glycogen synthase kinase-3 (GSK-3) inhibition in mitigating severe inflammation. The inhibition of GSK-3α/β by CHIR99021 promoted fetal lung progenitor proliferation and maturation of alveolar epithelial cells (AECs). The precise impact of CHIR99021 in lung repair and regeneration during acute lung injury (ALI) remains unexplored. This study intends to elucidate the influence of CHIR99021 on AEC behaviour during the peak of the inflammatory phase of ALI and, after its attenuation, during the repair and regeneration stage. Furthermore, a long-term evaluation was conducted post CHIR99021 treatment at a late phase of the disease. Our results disclosed the role of GSK-3α/β inhibition in promoting AECI and AECII proliferation. Later administration of CHIR99021 during ALI progression contributed to the transdifferentiation of AECII into AECI and an AECI/AECII increase, suggesting its contribution to the renewal of the alveolar epithelial population and lung regeneration. This effect was confirmed to be maintained histologically in the long term. These findings underscore the potential of targeted therapies that modulate GSK-3α/β inhibition, offering innovative approaches for managing acute lung diseases, mostly in later stages where no treatment is available. Full article
(This article belongs to the Special Issue Advanced Molecular Research in Lung Diseases)
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12 pages, 3010 KiB  
Article
Low Glucose plus β-Hydroxybutyrate Induces an Enhanced Inflammatory Response in Yak Alveolar Macrophages via Activating the GPR109A/NF-κB Signaling Pathway
by Jiancheng Qi, Qiyuan Yang, Qing Xia, Fangyuan Huang, Hongrui Guo, Hengmin Cui, Yue Xie, Zhihua Ren, Liping Gou, Dongjie Cai, Maqsood Ahmed Kumbhar, Jing Fang and Zhicai Zuo
Int. J. Mol. Sci. 2023, 24(14), 11331; https://doi.org/10.3390/ijms241411331 - 11 Jul 2023
Cited by 4 | Viewed by 2272
Abstract
Yaks are often subject to long-term starvation and a high prevalence of respiratory diseases and mortality in the withered season, yet the mechanisms that cause this remain unclear. Research has demonstrated that β-hydroxybutyrate (BHB) plays a significant role in regulating the immune system. [...] Read more.
Yaks are often subject to long-term starvation and a high prevalence of respiratory diseases and mortality in the withered season, yet the mechanisms that cause this remain unclear. Research has demonstrated that β-hydroxybutyrate (BHB) plays a significant role in regulating the immune system. Hence, we hypothesize that the low glucose and high BHB condition induced by severe starvation might have an effect on the pro-inflammatory response of the alveolar macrophages (AMs) in yaks. To validate our hypothesis, we isolated and identified primary AMs from freshly slaughtered yaks and cultured them in a medium with 5.5 mM of glucose or 2.8 mM of glucose plus 1–4 mM of BHB. Utilizing a real-time quantitative polymerase chain reaction (RT-qPCR), immunoblot assay, and enzyme-linked immunosorbent assay (ELISA), we evaluated the gene and protein expression levels of GPR109A (G-protein-coupled receptor 109A), NF-κB p65, p38, and PPARγ and the concentrations of pro-inflammatory cytokines interleukin (IL)-1β and IL-6 and tumor necrosis factor (TNF)-α in the supernatant. The results demonstrated that AMs exposed to low glucose plus BHB had significantly higher levels of IL-1β, IL-6, and TNF-α (p < 0.05) and higher activity of the GPR109A/NF-κB signaling pathway. A pretreatment of either pertussis toxin (PTX, inhibitor of GPR109A) or pyrrolidinedithiocarbamic (PDTC, inhibitor of NF-κB p65) was effective in preventing the elevated secretion of pro-inflammatory cytokines induced by low glucose plus BHB (p < 0.05). These results indicated that the low glucose plus BHB condition would induce an enhanced pro-inflammatory response through the activation of the GPR109A/NF-κB signaling pathway in primary yak AMs, which is probably the reason why yaks experience a higher rate of respiratory diseases and mortality. This study will offer new insight into the prevention and treatment of bovine respiratory diseases. Full article
(This article belongs to the Special Issue Advanced Molecular Research in Lung Diseases)
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Review

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28 pages, 1908 KiB  
Review
The Current Roadmap of Lung Cancer Biology, Genomics and Racial Disparity
by Enas S. Alsatari, Kelly R. Smith, Sapthala P. Loku Galappaththi, Elba A. Turbat-Herrera and Santanu Dasgupta
Int. J. Mol. Sci. 2025, 26(8), 3818; https://doi.org/10.3390/ijms26083818 - 17 Apr 2025
Viewed by 399
Abstract
Globally, lung cancer is the most prevalent cause of cancer-related death. There are two large histological groups of lung cancer: small-cell lung cancer (SCLC) and non-small-cell lung cancer (NSCLC). Based on histopathological and molecular features, adenocarcinoma (ADC) and squamous cell carcinoma (SCC) are [...] Read more.
Globally, lung cancer is the most prevalent cause of cancer-related death. There are two large histological groups of lung cancer: small-cell lung cancer (SCLC) and non-small-cell lung cancer (NSCLC). Based on histopathological and molecular features, adenocarcinoma (ADC) and squamous cell carcinoma (SCC) are the two major histologic subtypes of NSCLC. Various epidemiological and environmental factors are linked with an increased risk of lung cancer. However, these risk factors show disparities in patients with divergent racial and ethnic backgrounds. Interestingly, different populations were found to harbor distinct molecular features as evidenced by variations in genetic mutation profiles. Moreover, diverse histological and molecular progression patterns are identified in lung cancer, which could be crucial in improving diagnosis, prognosis, and therapeutic planning. In concert with a plethora of nuclear genetic alterations, mitochondrial alteration, epigenetic reprogramming, microbial dysbiosis, and immune alteration signatures have been identified in various lung cancer types. This review article provides a comprehensive overview of screening tests and the treatment strategies for NSCLC and SCLC, including surgery, radiation therapy, chemotherapy, targeted therapies, and immunotherapies. Through the unification of these diverse aspects, this review article aspires to a complete understanding of lung cancer’s genomics, biology, microbial landscapes, and racial disparity and seeks to understand the essential role of racial and ethnic factors in lung cancer occurrence and treatment. Full article
(This article belongs to the Special Issue Advanced Molecular Research in Lung Diseases)
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15 pages, 1068 KiB  
Review
A Comprehensive Outlook on Pulmonary Alveolar Proteinosis—A Review
by Julia Wołoszczak, Martyna Wrześniewska, Aleksandra Hrapkowicz, Kinga Janowska, Joanna Szydziak and Krzysztof Gomułka
Int. J. Mol. Sci. 2024, 25(13), 7092; https://doi.org/10.3390/ijms25137092 - 28 Jun 2024
Viewed by 2771
Abstract
Pulmonary alveolar proteinosis (PAP) is an ultra-rare disease caused by impaired pulmonary surfactant clearance due to the dysfunction of alveolar macrophages or their signaling pathways. PAP is categorized into autoimmune, congenital, and secondary PAP, with autoimmune PAP being the most prevalent. This article [...] Read more.
Pulmonary alveolar proteinosis (PAP) is an ultra-rare disease caused by impaired pulmonary surfactant clearance due to the dysfunction of alveolar macrophages or their signaling pathways. PAP is categorized into autoimmune, congenital, and secondary PAP, with autoimmune PAP being the most prevalent. This article aims to present a comprehensive review of PAP classification, pathogenesis, clinical presentation, diagnostics, and treatment. The literature search was conducted using the PubMed database and a total of 67 articles were selected. The PAP diagnosis is usually based on clinical symptoms, radiological imaging, and bronchoalveolar lavage, with additional GM-CSF antibody tests. The gold standard for PAP treatment is whole-lung lavage. This review presents a summary of the most recent findings concerning pulmonary alveolar proteinosis, pointing out specific features that require further investigation. Full article
(This article belongs to the Special Issue Advanced Molecular Research in Lung Diseases)
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