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Advances in Lung Research: From Mechanisms to Therapeutic Innovation
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Advances in Lung Research: From Mechanisms to Therapeutic Innovation

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 November 2026 | Viewed by 2907

Special Issue Editors

Prof. Dr. Johnatas D Silva

E-Mail Website
Guest Editor
1. Institute of Biomedical Science, Federal University of Rio de Janeiro, Rio de Janeiro 21941-590, RJ, Brazil
2. Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro 21941-902, RJ, Brazil
Interests: acute lung injury; lung inflammation; pathophysiology; molecular biology; cell therapy; mesenchymal stromal cells; extracellular vesicles; animal models; 3D models
Dr. Fernanda Ferreira Cruz

E-Mail Website
Guest Editor
Laboratory of Pulmonary Investigation, Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro 21941-902, RJ, Brazil
Interests: interstitial lung diseases; asthma; COPD; lung cancer; mesenchymal stromal cells; extracellular vesicles; mitotherapy

Special Issue Information

Dear Colleagues,

Remarkable advances in pulmonary science have expanded our understanding of the complex biological processes that regulate lung function and disease. From fundamental insights to molecular signalling, and from cell–cell communication to the development of novel therapeutic approaches, lung research now incorporates basic discovery, translational investigation, and personalized medicine.

For this Special Issue, “Advances in Lung Research: From Mechanisms to Therapeutic Innovation”, we invite original research articles and comprehensive reviews addressing the cellular and molecular pathways underlying lung injury, repair, and regeneration. We particularly welcome studies exploring pharmacological interventions, biologics, and stem cell-based therapies, as well as innovative experimental platforms such as precision-cut lung slices, organoid models, and lung-on-a-chip models to advance our mechanistic and translational understanding.

Submissions that specifically address mechanisms of injury and therapeutic strategies, from the molecular pathways underlying lung damage to innovative and personalized interventions, are strongly encouraged, as these themes can effectively bridge mechanistic understanding and clinical application. By integrating contributions from across basic, translational, and clinical researchers, this Special Issue will highlight the emerging concepts and technologies that are shaping the future of pulmonary medicine and driving the development of more effective, individualized treatments for lung diseases.

Prof. Dr. Johnatas D Silva
Dr. Fernanda Ferreira Cruz
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 250 words) can be sent to the Editorial Office for assessment.

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 disease
  • molecular mechanisms
  • lung injury and repair
  • regeneration
  • biomarkers
  • therapeutic innovation
  • translational research
  • personalized medicine

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Published Papers (4 papers)

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16 pages, 2660 KB  
Article
The Critical Role of Steroid Regimen for Lung Repair in Experimental Diffuse Alveolar Damage
by Aleksandr Chernov, Georgii Telegin, Evgeny Sinitsyn, Alexey Dmitriev, Viktor Palikov, Vitaly Kazakov, Maksim Rodionov, Igor Rybalkin, Tatiana Vlasik, Alexey Belogurov and Kirill Zykov
Int. J. Mol. Sci. 2026, 27(3), 1199; https://doi.org/10.3390/ijms27031199 - 25 Jan 2026
Cited by 1 | Viewed by 551
Abstract
Acute respiratory distress syndrome (ARDS) is a common condition among intensive care unit patients and is associated with high mortality. Currently, there are no unified therapeutic strategies, including for the use of systemic glucocorticosteroid (GCS) therapy, in the management of ARDS of various [...] Read more.
Acute respiratory distress syndrome (ARDS) is a common condition among intensive care unit patients and is associated with high mortality. Currently, there are no unified therapeutic strategies, including for the use of systemic glucocorticosteroid (GCS) therapy, in the management of ARDS of various etiologies. Using our previously developed non-surgical and reproducible model of unilateral total diffuse alveolar damage (ARDS/DAD) in the left lung of ICR mice, we investigated the effects of GCS with different durations of action and administration regimens on lung function recovery. Our data show that repeated-course administration of dexamethasone promoted complete normalization of respiratory function, as well as restoration of aeration and perfusion of the left lung in mice following ARDS/DAD induction. In contrast, a single administration of the same drug or the use of a prolonged-release formulation, despite exhibiting anti-inflammatory effects, did not provide adequate lung tissue recovery and, in some cases, even exacerbated injury. These results underscore that in ARDS therapy, not just the use but the specific dosing regimen of glucocorticoids is critically important for driving complete functional and structural lung repair. Full article
(This article belongs to the Special Issue Advances in Lung Research: From Mechanisms to Therapeutic Innovation)
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16 pages, 546 KB  
Review
Common Biomarkers in Chronic Obstructive Pulmonary Disease and Bronchopulmonary Dysplasia: A Narrative Review of an Intriguing Interplay
by Antonella Gambadauro, Federica Xerra, Valeria Chirico, Immacolata Rulli, Annalisa Cacciola, Raffaella Mallamace, Eloisa Gitto and Lucia Marina Marseglia
Int. J. Mol. Sci. 2026, 27(3), 1422; https://doi.org/10.3390/ijms27031422 - 30 Jan 2026
Viewed by 966
Abstract
Bronchopulmonary dysplasia (BPD) is a chronic lung condition in preterm infants characterized by impaired alveolar development, disrupted vascular growth, and persistent inflammation. These alterations, which often arise from early exposure to mechanical ventilation, oxygen toxicity, and infection, can lead to long-term structural and [...] Read more.
Bronchopulmonary dysplasia (BPD) is a chronic lung condition in preterm infants characterized by impaired alveolar development, disrupted vascular growth, and persistent inflammation. These alterations, which often arise from early exposure to mechanical ventilation, oxygen toxicity, and infection, can lead to long-term structural and functional deficits in the developing lung. In adulthood, chronic obstructive pulmonary disease (COPD) represents a major cause of morbidity and mortality and is defined by progressive airflow obstruction, reduced respiratory capacity, and chronic inflammatory responses. Although traditionally considered a disease of adult smokers, growing evidence suggests that early-life respiratory insults play a key role in shaping long-term lung health. Recent studies reveal a biologically plausible link between BPD and later COPD, indicating that premature birth, impaired lung growth, and early inflammatory injury may predispose individuals to earlier or more severe COPD development. This review explores the shared molecular pathways connecting these conditions, focusing on overlapping inflammatory biomarkers such as IL1B, IL6, IL8, TNF, TGFB, and VEGF, which collectively reflect persistent dysregulation of immune and repair mechanisms. Additionally, common genetic variants, including SERPINA1 and HHIP, may contribute to susceptibility across the lifespan. Emerging biomarkers—such as PRMT7, cathelicidin/LL-37, CRISPLD2, and GDF15—offer further insight into disease progression. Identifying these shared markers may ultimately improve early detection and help clinicians pinpoint infants with BPD who face an elevated risk of developing COPD later in life. Full article
(This article belongs to the Special Issue Advances in Lung Research: From Mechanisms to Therapeutic Innovation)
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19 pages, 5423 KB  
Article
Mitochondrial Transplantation from Bone Marrow Mesenchymal Stromal Cells Combined with Sildenafil Attenuated Vascular Remodeling and Improved Right Ventricular Dysfunction in Experimental Pulmonary Arterial Hypertension
by Maria E. de S. F. Onofre, Renata T. Santos, Nazareth de N. Rocha, Dayene de A. F. Caldeira, Johnatas D. Silva, Carla M. da Silva, Monique M. Melo, Mayck M. A. da Silva, Clara R. S. Pastor, Julia D. Batista, Isadora A. Botelho, Rodrigo G. Veras, Sabrina S. de S. Serra, Julianna D. Zeidler, Patricia R. M. Rocco, Fernanda F. Cruz and Pedro L. Silva
Int. J. Mol. Sci. 2026, 27(4), 1761; https://doi.org/10.3390/ijms27041761 - 12 Feb 2026
Viewed by 927
Abstract
Pulmonary arterial hypertension (PAH) is characterized by progressive vascular remodeling and right ventricular (RV) dysfunction, processes that are increasingly associated with disturbances in cellular metabolism. We investigated whether transplantation of exogenous mitochondria derived from bone marrow mesenchymal stromal cells, alone or combined with [...] Read more.
Pulmonary arterial hypertension (PAH) is characterized by progressive vascular remodeling and right ventricular (RV) dysfunction, processes that are increasingly associated with disturbances in cellular metabolism. We investigated whether transplantation of exogenous mitochondria derived from bone marrow mesenchymal stromal cells, alone or combined with sildenafil, could improve mitochondrial homeostasis and attenuate cardiopulmonary remodeling in monocrotaline-induced PAH. Male Wistar rats were assigned to control (CTRL, n = 8) or PAH (n = 32) groups. Fourteen days after induction of PAH, animals were randomized to receive saline, sildenafil (20 mg/kg/day for 14 days), intravenous mitochondrial transplantation (100 μg, days 14 and 21), or combined therapy. On day 28, echocardiography, invasive measurement of RV systolic pressure (RVSP), pulmonary vascular histology, gene expression analyses (vimentin, VE-cadherin, and mitochondrial metabolism–related genes), and high-resolution respirometry were performed. All treatments significantly reduced RVSP compared with untreated PAH. Mitochondrial therapy, alone or combined with sildenafil, decreased arteriolar α-smooth muscle actin content, whereas endothelial–mesenchymal transition was attenuated only with combined treatment. Mitochondrial transplantation and sildenafil increased Complex I–dependent respiration, whereas Complex IV activity improved exclusively with mitochondrial therapy. Combined treatment reduced plasma IL-6 and IL-1β levels compared with PAH. Thus, mitochondrial transplantation, particularly when combined with sildenafil, improved RV function, limited pulmonary vascular remodeling, reduced plasma inflammatory markers, and changed key mitochondrial pathways in experimental PAH. Full article
(This article belongs to the Special Issue Advances in Lung Research: From Mechanisms to Therapeutic Innovation)
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25 pages, 4201 KB  
Article
From Mechanisms to Therapeutic Innovation in Non-Small-Cell Lung Cancer: A Knowledge-Depth Translational Mapping with Experimental Validation
by Aimi Syamima Abdul Manap
Int. J. Mol. Sci. 2026, 27(12), 5245; https://doi.org/10.3390/ijms27125245 - 10 Jun 2026
Viewed by 140
Abstract
Background: Non-small-cell lung cancer (NSCLC) research has transitioned from tumor-intrinsic mechanisms to immune-driven therapeutic innovation; however, the translation of mechanistic insights into clinically actionable strategies remains incompletely defined. Methods: A total of 1213 records were retrieved from the Web of Science Core Collection [...] Read more.
Background: Non-small-cell lung cancer (NSCLC) research has transitioned from tumor-intrinsic mechanisms to immune-driven therapeutic innovation; however, the translation of mechanistic insights into clinically actionable strategies remains incompletely defined. Methods: A total of 1213 records were retrieved from the Web of Science Core Collection (SCI-Expanded) (2009–2025). After data cleaning and duplicate removal (n = 13), 1200 publications were analyzed. Bibliometrix (R) and CiteSpace were used for performance analysis, keyword mapping, thematic evolution, and co-citation clustering. Results: Annual scientific production increased markedly after 2018, paralleling the expansion of immunotherapy. Keyword co-occurrence identified three major thematic domains (>40 high-frequency keywords) linking molecular mechanisms, biomarkers, and therapeutic strategies. Thematic mapping highlighted immunotherapy, tumor microenvironment, and PD-1 as dominant motor themes, while resistance-related pathways formed a central mechanistic–translational axis. Thematic evolution demonstrated a shift from EGFR-targeted therapy to epithelial–mesenchymal transition (EMT)-centered resistance and subsequently to immune-dominant strategies. Co-citation clustering produced robust structures (Q ≈ 0.62; silhouette ≈ 0.84), identifying EMT as a persistent mechanistic hub. Pilot ELISA validation confirmed significant increases in TGF-β1 (~2.05-fold), IL-6 (~2.59-fold), CCL2 (~2.10-fold), and PD-L1 (~2.56-fold) under EMT-inducing conditions (p < 0.01). Conclusions: This integrative approach provides a quantitative and experimentally supported framework linking mechanistic insights to therapeutic innovation in NSCLC. Full article
(This article belongs to the Special Issue Advances in Lung Research: From Mechanisms to Therapeutic Innovation)
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