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Navigating the Complex Landscape of Non-Communicable Respiratory Diseases: Emerging Challenges...
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Navigating the Complex Landscape of Non-Communicable Respiratory Diseases: Emerging Challenges and Opportunities

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 31 October 2026 | Viewed by 7735

Editor

Prof. Dr. Katya Rigatto

E-Mail Website
Guest Editor
Departamento de Ciências Básicas da Saúde, Laboratório de Fisiologia Translacional, Universidade Federal de Ciências da Saúde de Porto Alegre, Porto Alegre, Brazil
Interests: hypertension; pulmonary; angiotensin; lung disease; pulmonary arterial hypertension

Special Issue Information

Dear Colleagues,

This Special Issue explores the complex interplay of genetic, environmental, and pathophysiological factors in non-communicable respiratory diseases, such as asthma, idiopathic pulmonary fibrosis (IPF), and chronic obstructive pulmonary disease (COPD), among others. Despite their distinct manifestations, they share common pathways like inflammation, which connect their pathophysiology. Asthma involves genetic and environmental interactions leading to airway inflammation, requiring personalized treatment with emerging biomarkers and therapies. IPF and COPD are similarly affected by environmental factors such as air pollution, especially particulate matter, which exacerbates disease progression through respiratory and systemic inflammation. Recent studies indicate potential roles for the renin–angiotensin system in these diseases, offering new therapeutic targets. These conditions present significant public health challenges, incurring substantial economic costs from healthcare and productivity losses. Global challenges, such as increasing urbanization and lifestyle changes, further disrupt immune responses and compromise epithelial integrity, promoting these diseases. Understanding these pathways is essential for comprehensive strategies addressing biological and socioeconomic determinants of respiratory health. This area of research highlights the need for a multifaceted approach to managing these diseases, integrating innovative therapies and biomarker development to enhance patient outcomes and resilience amidst evolving global circumstances. We look forward to your contributions.

Prof. Dr. Katya Rigatto
Guest Editor

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Keywords

  • non-communicable respiratory diseases
  • asthma
  • idiopathic pulmonary fibrosis
  • chronic obstructive pulmonary disease

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Published Papers (6 papers)

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Research

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18 pages, 18415 KB  
Article
Wnt/Chemerin Signaling Involved in Exercise Training Preventing Diaphragm Dysfunction Induced by Cigarette Smoke
by Peijun Li, Jian Li, Yingqi Wang, Xiaoyu Han, Yuanyuan Cao, Meiling Jiang, Yidie Bao, Weibing Wu and Xiaodan Liu
Biomedicines 2026, 14(6), 1382; https://doi.org/10.3390/biomedicines14061382 - 18 Jun 2026
Viewed by 272
Abstract
Objectives: The current study examined whether exercise training alleviates cigarette smoke (CS)-induced diaphragm dysfunction by modulating inflammation through the Wnt and Chemerin signaling pathways. Methods: Mechanical stretching was applied for 3 consecutive days to explore the effects on cell proliferation and [...] Read more.
Objectives: The current study examined whether exercise training alleviates cigarette smoke (CS)-induced diaphragm dysfunction by modulating inflammation through the Wnt and Chemerin signaling pathways. Methods: Mechanical stretching was applied for 3 consecutive days to explore the effects on cell proliferation and chemerin/chemokine-like receptor 1 (CMKLR1) expression in C2C12 cells pretreated with lipopolysaccharide. Male wild-type (WT) and CMKLR1 knockout (KO) mice (6–8 weeks old) were exposed to CS for 6 months (1–2 h a day, 6 days a week) to determine the role of chemerin/CMKLR1 in the progression of diaphragm dysfunction. Given that Wnt/β-catenin is a potential modulator of chemerin/CMKLR1, its expression was detected in CS-exposed mice and mice subjected to treadmill exercise training after CS exposure. Wnt/β-catenin agonist lithium chloride (LiCl) and antagonist XAV939 were then intraperitoneally injected into the CS-exposed mice during exercise training to further investigate their potential synergistic effects with exercise training on improving CS-induced diaphragm dysfunction. Isolated diaphragm contraction strength and fiber cross-sectional area were measured to determine the diaphragm dysfunction. Results: Mechanical stretching improved the proliferation level of myoblasts and decreased inflammation and CMKLR1 protein expression (p < 0.05). The KO mice showed diminished diaphragm dysfunction compared with the WT mice after long-term CS exposure. Combined LiCl and exercise training further enhanced the improvement of diaphragmatic isolated strength in mice exposed to CS (p < 0.01), activated the protein degradation and synthesis pathways, and decreased IL-1β level (p < 0.05). Combined XAV939 and exercise training significantly decreased chemerin protein level (p < 0.01). Conclusions: Exercise training can downregulate inflammation levels and improve diaphragm dysfunction in CS-exposed mice, partially by enhancing Wnt expression and reducing abnormally activated chemerin. Full article
(This article belongs to the Special Issue Navigating the Complex Landscape of Non-Communicable Respiratory Diseases: Emerging Challenges and Opportunities)
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18 pages, 921 KB  
Article
Idiopathic Pulmonary Fibrosis: Analysis of Predisposing Variants in Patients with Familial Forms
by Ilaria Stanghellini, Elena Bonora, Marco Sebastiani, Carlo Salvarani, Filippo Gozzi, Dario Andrisani, Roberto Tonelli, Nicola Rizzardi, Christian Bergamini, Federica Isidori, Marco Seri, Enrico Clini, Stefania Cerri and Olga Calabrese
Biomedicines 2026, 14(1), 138; https://doi.org/10.3390/biomedicines14010138 - 9 Jan 2026
Viewed by 1288
Abstract
Background: idiopathic pulmonary fibrosis (IPF) causes progressive and irreversible changes in the lung parenchyma, leading to respiratory failure. Its pathogenesis involves several damage/repair mechanisms leading to fibrosis, whilst alterations of genes implicated in these processes contribute to the development of the disease. [...] Read more.
Background: idiopathic pulmonary fibrosis (IPF) causes progressive and irreversible changes in the lung parenchyma, leading to respiratory failure. Its pathogenesis involves several damage/repair mechanisms leading to fibrosis, whilst alterations of genes implicated in these processes contribute to the development of the disease. At present, next-generation sequencing (NGS) analyses investigate single-nucleotide or small indel variants, and no evaluation of genomic rearrangements has been so far reported. Methods: In order to identify predisposing variants, we analyzed—both by NGS and by comparative genomic hybridization/single-nucleotide polymorphism (CGH-SNP array) array—37 patients with a diagnosis of familial pulmonary fibrosis. Results: a total of 17 patients (46%) harbored copy number variations (CNVs), 10 (27%) did not harbor any CNVs, 5 (13.5%) showed a mosaic deletion of the Y chromosome, and 5 (13.5%) showed a run of homozygosity (ROH). NGS identified causative variants (including a novel one) in five patients (5/37, 13.5%) and confirmed the high prevalence of MUC5B promoter polymorphism rs35705950, including the detection of a previously unreported form in IPF SNP (indicated as “novel” in the main text), rs141420125 (23/37; 62%). Conclusions: CGH-SNP array identified CNVs containing genes involved in mechanisms (i.e., oxidative stress, mitophagy, NF-Kb pathway) that have been shown to play a role in the pathogenesis of IPF. Therefore, the application of CGH-SNP array or other quantitative tests should be considered in the diagnostic setup of these patients Full article
(This article belongs to the Special Issue Navigating the Complex Landscape of Non-Communicable Respiratory Diseases: Emerging Challenges and Opportunities)
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11 pages, 408 KB  
Article
Analysis of the Relationship Between CHRNA3/5 and EPHX1 Polymorphisms to Tobacco Intake and Development of Chronic Obstructive Pulmonary Disease (COPD)
by Thiago Prudente Bartholo, Luis Cristóvão Porto, Roberto Pozzan, Adriana Nascimento, Barbara Beatriz Garcia Raskovisch Bartholo, Rogerio Rufino and Cláudia Henrique da Costa
Biomedicines 2025, 13(11), 2781; https://doi.org/10.3390/biomedicines13112781 - 14 Nov 2025
Viewed by 831
Abstract
Background: Chronic obstructive pulmonary disease (COPD) is a complex condition influenced by both environmental and genetic factors. Among the genetic determinants, polymorphisms in the CHRNA3/5 and EPHX1 genes have been implicated in nicotine dependence and susceptibility to COPD in several populations. However, evidence [...] Read more.
Background: Chronic obstructive pulmonary disease (COPD) is a complex condition influenced by both environmental and genetic factors. Among the genetic determinants, polymorphisms in the CHRNA3/5 and EPHX1 genes have been implicated in nicotine dependence and susceptibility to COPD in several populations. However, evidence remains limited in admixed populations such as Brazilians. Methods: This cross-sectional study investigated the association between CHRNA3 (rs1051730, rs8034191) and EPHX1 (rs2234922) polymorphisms with tobacco nicotine dependence and COPD in a Brazilian cohort. Genotyping was performed using TaqMan® SNP assays, and pulmonary function was assessed via spirometry according to ATS/ERS standards. Associations between genetic variants, tobacco intake, and COPD status were evaluated using χ2 and Fisher’s exact tests, with odds ratios (ORs) and 95% confidence intervals (CIs). Post hoc power analyses were conducted to estimate detectable effect sizes. Results: A total of 123 active or former smokers were analyzed. The CHRNA3 variants (rs1051730 and rs8034191) showed a trend toward higher prevalence among individuals with heavy tobacco intake (>40 pack-years), though no significant allelic or genotypic differences were found between COPD and control groups (p > 0.05). The EPHX1 rs2234922 A allele was significantly more frequent in COPD patients, suggesting increased disease risk (p < 0.05), while the GG genotype appeared protective. Post hoc power analyses indicated moderate power (≈0.56–0.63) for the observed associations. Conclusions: In this Brazilian population, the CHRNA3/5 polymorphisms may influence nicotine dependence, while EPHX1 rs2234922 appears to be associated with COPD susceptibility. These findings support a potential genetic contribution to disease risk and tobacco nicotine dependence, warranting further large-scale studies to confirm these associations and explore their therapeutic implications. Full article
(This article belongs to the Special Issue Navigating the Complex Landscape of Non-Communicable Respiratory Diseases: Emerging Challenges and Opportunities)
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12 pages, 273 KB  
Article
Effects of Antifibrotic Therapy in Patients with Combined Pulmonary Fibrosis and Emphysema: A US-Based Cohort Study
by Abhishek Shah, Esteban Kosak Lopez, Andrew Geller, Maanav Patel and Sadia Benzaquen
Biomedicines 2025, 13(10), 2522; https://doi.org/10.3390/biomedicines13102522 - 16 Oct 2025
Cited by 1 | Viewed by 1615
Abstract
Background/Objectives: Combined pulmonary fibrosis and emphysema (CPFE) is associated with poor outcomes. We investigated the association of antifibrotic therapy on patients with CPFE. Methods: This retrospective study included adult patients, older than 18 years, with a diagnosis of CPFE between 2015 [...] Read more.
Background/Objectives: Combined pulmonary fibrosis and emphysema (CPFE) is associated with poor outcomes. We investigated the association of antifibrotic therapy on patients with CPFE. Methods: This retrospective study included adult patients, older than 18 years, with a diagnosis of CPFE between 2015 and 2019 using TrinetX database. CPFE was defined as a diagnosis of pulmonary fibrosis (PF) and emphysema or chronic obstructive pulmonary disease. Propensity score matching was performed to compare baseline characteristics for CPFE patients on antifibrotic therapy (nintendanib and pirfenidone) with those not on antifibrotic therapy. The outcomes studied included all-cause mortality, major adverse cardiac event (MACE, [myocardial infarction, unstable angina]), hypoxic and hypercapnic respiratory failure, and stroke. These outcomes were compared at one-, three-, and five-year follow-ups. Results: Patients were divided into two cohorts: those on antifibrotic therapy (cohort 1, n = 861) and those without antifibrotic therapy (cohort 2, n = 861). Although not statistically significant, there was a trend towards increased mortality in cohort 1 at the 5-year follow-up (HR 1.14; CI 0.99–1.33). There was also an increased incidence of MI (HR 1.68; CI 0.88–1.47) and hypoxic respiratory failure (HR 1.17; CI 0.99–1.39). Notably, there was also a trend towards decreased incidence of stroke (HR 0.73; CI 0.51–1.05), and no difference in unstable angina (HR 0.94; CI 0.47–1.86) and hypercapnic respiratory failure (HR 0.99; CI 0.67–1.47). Conclusions: For patients with CFPE, antifibrotic use demonstrated a trend towards increased risk of mortality at 5-year follow-up, raising concerns for “sicker patient” bias. Prospective studies should be designed to include patients with CPFE and evaluate the benefits of antifibrotics. Full article
(This article belongs to the Special Issue Navigating the Complex Landscape of Non-Communicable Respiratory Diseases: Emerging Challenges and Opportunities)
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15 pages, 2435 KB  
Article
Localization and Expression of Renin–Angiotensin System Receptors in Lung from Transplant Patients: A Case-Control Study
by Andresa Thomé Silveira, Lucas Sagrillo Fagundes, Juliane Flor, Isabel Amaral Martins, Laura Bastos Otero, Laura Tibola Marques da Silva, Lorenzo Santana Maciel, Sarah Eller, Giuliano Rizzotto Guimarães, Fabíola Adelia Perin, Márcia Rosângela Wink and Katya Rigatto
Biomedicines 2025, 13(9), 2312; https://doi.org/10.3390/biomedicines13092312 - 21 Sep 2025
Cited by 2 | Viewed by 1090
Abstract
Objective: We aimed to assess the expression and localization of renin-angiotensin system (RAS) receptors in lung tissue and the plasma concentration of related peptides in IPF patients. Materials and Methods: This case–control study involved 19 patients from southern Brazil undergoing lung [...] Read more.
Objective: We aimed to assess the expression and localization of renin-angiotensin system (RAS) receptors in lung tissue and the plasma concentration of related peptides in IPF patients. Materials and Methods: This case–control study involved 19 patients from southern Brazil undergoing lung resection or transplantation. Plasma levels of Angiotensin I, II, A, 1-7, Alamandine were measured via liquid chromatography–tandem mass spectrometry. Lung tissue expression and localization of angiotensin type 1 (AT1), Mas, and Mas-related G-protein-coupled receptor D (MrgD) receptors were evaluated using Western blot and immunohistochemistry. Clinical data and the 6-min walk test were analyzed to correlate receptor expression with lung function and oxygen dependence. Results: IPF patients showed reduced forced vital capacity (FVC) at 49 ± 13% and forced expiratory volume (FEV1) at 51 ± 14%, with a 60% increase in oxygen dependence. Plasma peptide concentrations were similar between the groups, except for Angiotensin I, which was significantly higher in the control group. In IPF lungs, AT1 and Mas receptors were expressed 2.31 and 2.13 times more, respectively, while MrgD expression was lower. Mas receptors were mostly found in bronchiole areas, whereas MrgD was predominant in the lung parenchyma. Conclusions: This study indicates that the RAS operates independently within tissue, in addition to its systemic functions, highlighting distinct differences between tissue and plasma RAS activities. The distinct roles of MrgD and Mas receptors in lung structure and function could be pivotal for new therapies, potentially leading to more effective IPF treatments. Full article
(This article belongs to the Special Issue Navigating the Complex Landscape of Non-Communicable Respiratory Diseases: Emerging Challenges and Opportunities)
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Review

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18 pages, 1828 KB  
Review
From Inflammation to Precision Medicine: Mechanistic Insights into Asthma, COPD, and IPF
by Najla Ghrairi, Youssef Zied Elhechmi and Soumaya Ben Saad
Biomedicines 2026, 14(5), 1055; https://doi.org/10.3390/biomedicines14051055 - 7 May 2026
Viewed by 1063
Abstract
Asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF) are major non-communicable respiratory diseases (NCD-RDs) with high morbidity and mortality. Despite distinct clinical features, they share overlapping mechanisms including oxidative stress, epithelial injury, and immune dysregulation. Asthma is mainly driven by [...] Read more.
Asthma, chronic obstructive pulmonary disease (COPD), and idiopathic pulmonary fibrosis (IPF) are major non-communicable respiratory diseases (NCD-RDs) with high morbidity and mortality. Despite distinct clinical features, they share overlapping mechanisms including oxidative stress, epithelial injury, and immune dysregulation. Asthma is mainly driven by type 2 inflammation, with IL-4, IL-5, and IL-13 inducing eosinophilia, IgE production, mucus hypersecretion, and airway remodeling. Biologics targeting IgE, IL-5, and IL-4Rα have transformed treatment, and agents directed against TSLP and IL-33 further extend the range of targeted interventions. In contrast, COPD involves chronic inflammation with macrophages, neutrophils, and CD8+ T cells, persisting after smoking cessation. Advances include biologics such as dupilumab and benralizumab in eosinophilic COPD, and novel inhaled therapies such as ensifentrine, the first dual PDE3/4 inhibitor delivered via inhalation. IPF, on the other hand, arises from defective epithelial repair and fibroblast activation, causing progressive fibrosis. Approved antifibrotics (nintedanib, pirfenidone) slow lung function decline, while new strategies target TGF-β, CTGF, and fibroblast-directed pathways. Across these diseases, biomarkers and the treatable traits framework are reshaping precision care. Personalized approaches integrating biomarkers, omics, and targeted therapies represent the most promising path for improved outcomes. Full article
(This article belongs to the Special Issue Navigating the Complex Landscape of Non-Communicable Respiratory Diseases: Emerging Challenges and Opportunities)
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