Search Results (4,592)

Background: MicroRNAs (miRNAs) are stable, small non-coding RNAs involved in asthma-related pathways and are promising diagnostic biomarkers and therapeutic targets in childhood asthma. Objective: To identify miRNAs differentially expressed in preschool wheezing and childhood asthma, evaluate their association with asthma diagnosis and severity-related phenotypes, and explore their potential translational relevance through exploratory bioinformatic analyses. Methods: A systematic search of Medline, Embase, SCOPUS, PubMed, CINAHL, and Web of Science was conducted for English-language articles published up to March 19, 2025. Eligible human studies reported that miRNAs were differentially expressed in children with wheeze or asthma versus healthy controls (p < 0.05, fold change ≥ 1.5). Bioinformatic analysis identified hub genes, constructed protein–protein interaction networks, and predicted drug–gene interactions. Results: Forty-seven studies met the inclusion criteria, yielding 58 differentially expressed miRNAs (31 up, 27 down). Recurrently reported miRNAs included miR-497, let-7e, miR-98, miR-21, miR-126a, miR-196a2, miR-1, miR-146a-5p, miR-210-3p, miR-145-5p, and miR-200c-3p across blood, nasal swabs, BALF, and exhaled breath condensate. miR-26a showed strong diagnostic performance (sensitivity 83%, specificity 93%; p < 0.002, 95% CI 0.831–0.987). Functional enrichment implicated 56 differentially expressed genes in metabolic and immune processes. Ten hub genes (including TNF, IL5, IL13, TLR4) were linked to 339 potential therapeutic agents; the exploratory network analysis highlighted overlap between predicted miRNA-regulated hub genes and existing asthma-relevant drug targets, including approved biologics. Conclusions: Our review findings suggest that several miRNAs are promising candidate biomarkers for childhood asthma phenotyping and severity assessment; however, their diagnostic utility remains exploratory and requires rigorous external validation and standardisation before clinical application. Full article

Background: Clinical remission has become a realistic treatment goal in severe asthma, but current evidence mostly reports global remission rates without accounting for baseline disease burden. No simple tool exists to quantify baseline severity and estimate an individual patient’s probability of achieving remission under biologic therapy. Methods: This prospective observational study included 93 adults with severe asthma initiating tezepelumab across 14 specialised severe asthma units in Spain. Four baseline domains—poor symptom control (ACT < 20), ≥1 severe exacerbation in the previous 12 months, maintenance oral corticosteroid (OCS) use, and FEV₁ < 80% predicted—were used to construct an empirically weighted composite score (Base4Score) based on the inverse probability of correcting each abnormal domain at 12 months. Strict clinical remission at 12 months was defined as ACT ≥ 20, no severe exacerbations, no maintenance OCS, and FEV₁ ≥ 80%. Logistic regression was used to assess the association between the score and non-remission, adjusting for age, sex, smoking status, T2 phenotype, and biologic-naive status. Results: Of 93 treated patients, 81 had complete baseline data for Base4Score derivation and 77 had complete 12-month data for strict clinical remission analysis. Strict clinical remission was achieved in 16/77 patients (20.8%). Remission rates decreased across increasing baseline score strata: 40.0% for scores < 5, 17.6% for scores 5 to <9, and 12.5% for scores ≥ 9 (linear p-trend = 0.022). Each 1-point increase in the continuous Base4Score was associated with higher adjusted odds of non-remission (OR 1.22; 95% CI 1.00–1.49; p = 0.047), and patients with scores ≥ 9 had approximately sevenfold higher adjusted odds of non-remission than those with scores < 5 (OR 6.77; 95% CI 1.40–32.84; p = 0.018). Conclusions: The Base4Score is a simple, empirically derived baseline severity index that predicts 12-month strict clinical remission in severe asthma treated with tezepelumab. If externally validated, it could help personalise expectations, optimise timing of biologic initiation and guide treat-to-target strategies in severe asthma. Full article

Modeling immune cell recruitment within a wound-relevant microenvironment remains challenging. Here, we developed a novel skin-derived extracellular matrix (ECM) hydrogel model to study monocyte (THP-1) entry and phenotypic changes within a dermal fibroblast-populated (NHDF) matrix. The main novelty of this study is that it compares the effects of fibroblast-derived soluble signals and active monocyte infiltration in a 3D biomimetic model. Signaling by fibroblast-secreted soluble factors enhanced a pro-angiogenic secretome (e.g., >3-fold upregulation of VEGFA at day 1) and promoted endothelial tube formation (increasing network junctions to 1.16 ± 0.16 vs. 0.93 ± 0.23 in monoculture). In contrast, this paracrine signaling did not induce the matrix-driven pro-fibrotic response in hydrogels. Crucially, physical immune infiltration restricted monocyte penetration (mean depth of 8.92 ± 2.27 μm vs. 121.1 ± 15.9 μm in monoculture at day 5), reduced hydrogel-induced myofibroblast activation (decreasing α-SMA+ cells from 79.1% to 54.3% upon initial contact), and was associated with slower collagen loss during the early phase. (retaining a high-density collagen ratio of 3.46 ± 0.33 vs. 2.02 ± 0.29 in monoculture at day 1). These observations were accompanied by a shift toward a matrix-stabilizing profile, including increased TIMP expression and reduced pro-fibrotic markers. (ACTA2 and COL1A1). By including active immune infiltration (which was absent in previous tSVF models), we capture the transition from inflammation to the proliferation stage. Although the later stages of extensive ECM remodeling appear suppressed here, they may occur as repair progresses. Overall, our findings highlight that the immune cell is a key regulatory component for coordinating matrix preservation and vascular support. Importantly, this model replicates the early phases of wound healing, a stage where the monocyte–fibroblast secretome supports endothelial network formation. We established this innovative 3D ECM hydrogel system as a practical and physiologically relevant platform to investigate immune–matrix–stromal crosstalk. Full article

Interest in artificial intelligence (AI) is rapidly growing. In healthcare, especially through machine learning and deep learning, AI is emerging as a promising tool to support the diagnosis, management, and prevention of lung diseases and to advance personalized care, although it requires large, well-structured datasets. Clinicians must learn how to integrate AI into routine practice for conditions such as asthma and chronic obstructive pulmonary disease (COPD), while ensuring patient safety and building trust in these tools. Chronic respiratory diseases are major global causes of morbidity and mortality and place a substantial burden on healthcare systems; among them, asthma and COPD are chronic disorders characterized by airway obstruction and inflammation. This review highlights the rapid advancement of AI, and it aims to explore the literature’s evidence of its applicability in controlling chronic respiratory disorders, particularly in asthma and COPD. We conducted a narrative literature review by searching ScienceDirect, PubMed, and Google Scholar for English-language studies on artificial intelligence applications in asthma and COPD and by screening the references of relevant articles. The reviewed literature suggests that AI-based approaches are being applied across the asthma–COPD spectrum to support diagnosis and phenotyping, improve risk stratification and prediction of clinically relevant outcomes, and enable more continuous monitoring using heterogeneous data sources (e.g., clinical records, imaging, and digital health data). AI-based tools are poised to support clinicians in asthma and COPD across diagnosis, phenotyping, and monitoring; however, their safe implementation in routine care will require robust validation, transparency, and governance to ensure reliability and patient safety. Full article

Background: Severe asthma remains associated with substantial morbidity despite optimized inhaled therapy. Biologic agents targeting type 2 inflammation improve clinical outcomes; however, real-world evidence regarding the durability of these effects beyond the first treatment year remains limited. The present study extends the follow-up of a previously reported real-world cohort in which 12-month outcomes of biologic therapy were evaluated. Methods: We conducted a retrospective observational longitudinal study of adults with severe asthma treated with omalizumab, benralizumab, or dupilumab at a tertiary center in Târgu-Mureș, Romania, between 2020 and 2025, extending follow-up of a previously published real-world cohort. The same patient cohort was followed for an additional period, with longitudinal data collected up to 24 months after biologic therapy initiation. Clinical, functional, and biomarker outcomes were assessed at baseline, 12 months, and 24 months, including Asthma Control Test (ACT) score, forced expiratory volume in one second (FEV₁% predicted), annual exacerbation rate, blood eosinophil count, and fractional exhaled nitric oxide (FeNO). Remission was defined as clinical (ACT ≥ 20, no severe exacerbations, and no maintenance oral corticosteroids), biological (FeNO < 20 ppb and blood eosinophils < 150/µL), and complete (both clinical and biological). Longitudinal changes were analyzed using the Friedman test with post hoc Wilcoxon signed-rank tests. Results: Forty-eight patients were included at baseline, and 41 had available data at 24 months. ACT scores improved from 12 (IQR 11–14) at baseline to 23 (21–25) at 12 months and remained stable at 22 (20–25) at 24 months (p < 0.001). Predicted FEV₁% increased from 50 (39–59) to 78 (68–88) at 12 months and 79 (66–96) at 24 months (p < 0.001). Blood eosinophil counts were markedly suppressed, and FeNO levels continued to decrease over time. Exacerbations declined from 2 (2–3) per year at baseline to 0 and 0.5 (0–1) at 12 and 24 months, respectively (p < 0.001). At 24 months, clinical, biological, and complete remission were observed in 61.0%, 78.0%, and 41.5% of patients with available paired data, respectively. Conclusions: Biologic therapy was associated with sustained clinical and functional improvement over 24 months, accompanied by sustained improvement in type 2 airway inflammation and increasing proportions of patients meeting remission criteria in real-world practice. Full article

Dendritic cells (DCs) are key sentinels in the lung mucosa that interpret environmental signals to either promote tolerance or trigger inflammation, influencing the development of chronic lung diseases. This review highlights recent mechanistic insights showing that metabolic checkpoints serve as upstream regulators of DC fate and activity: inflammatory stimuli activate HIF-1α/mTOR-linked glycolytic pathways that drive maturation, cytokine secretion, antigen presentation, and migration. In contrast, AMPK-related oxidative and lipid metabolism pathways support tolerogenic states that encourage regulatory T-cell responses and inhibit checkpoints like PD-1/PD-L1. We also present evidence that DC subset specialization (cDC1 vs. cDC2) and their tissue location interact with these metabolic pathways to regulate lymphoid tissue formation, including the development and persistence of tertiary lymphoid structures in chronically inflamed lungs. These ectopic lymphoid tissues enhance local immune responses through DC–stromal interactions and ongoing T follicular helper–B cell communication, contributing to persistent inflammation and tissue remodeling in conditions such as COPD, asthma, pulmonary hypertension, and fibrotic interstitial lung disease. Finally, we discuss the translational potential of targeting this immunometabolic–lymphoid pathway, suggesting that modulating metabolic regulators, migratory circuits, and tolerogenic programs could restore immune balance while maintaining host defense—a promising framework for developing advanced therapies for chronic lung inflammation. Full article

Ragweed (Ambrosia artemisiifolia) represents a major and expanding source of aeroallergen exposure in Europe, with rising sensitization rates and substantial clinical impact. However, population-level data integrating airborne pollen exposure with detailed clinical sensitization patterns remain limited. We conducted a 5-year retrospective cross-sectional observational analysis of sensitization prevalence, complemented by a parallel temporal analysis of aerobiological data and symptom-driven healthcare presentation patterns (2020–2024) in Timisoara, Romania, including all patients undergoing first-time sensitization evaluation at a tertiary referral hospital. Sensitization was assessed using standardized skin prick testing to common aeroallergens and other allergen categories, while airborne ragweed pollen concentrations were monitored through a peri-urban network of real-time bio-particle analyzers. Statistical analyses included descriptive statistics, multivariable logistic regression, χ² tests for co-sensitization patterns, and comparative analyses of clinical manifestations across sensitization profiles. Among 4404 eligible patients, 50.7% were sensitized to at least one allergen. Ragweed sensitization was identified in 24.1% of patients, with a mean age of 31.1 years at diagnosis and no significant sex-related difference. Most ragweed-sensitized patients were polysensitized (71.5%), predominantly to other aeroallergens. Increasing age was independently associated with lower odds of polysensitization to other aeroallergens (adjusted OR = 0.97 per year, 95% CI: 0.96–0.98), while sex showed no independent association. Patients with ragweed sensitization alone and those cosensitized with aeroallergens exhibited similar prevalence of respiratory manifestations, whereas individuals with additional non-aeroallergen sensitization showed lower prevalence of rhinitis, conjunctivitis, and asthma but slightly higher rates of asthma exacerbations. Weekly diagnoses of ragweed sensitization demonstrated a pronounced seasonal peak between calendar weeks 33 and 38 (mid-August to late September), coinciding with peak airborne ragweed pollen concentrations. Ragweed sensitization therefore represents a substantial and seasonally driven healthcare burden in western Romania, characterized by frequent polysensitization, distinct clinical manifestation patterns across sensitization profiles, and close temporal alignment between airborne pollen exposure and clinical presentation. Integrating aerobiological monitoring with clinical surveillance may support targeted prevention strategies and improved patient management. Full article

Transient receptor potential vanilloid 4 (TRPV4) is a polymodal cation channel that is widely expressed in sensory neurons, immune cells, and structural tissues, where it integrates mechanical, osmotic, and chemical stimuli to regulate both physiological responses and disease-associated signaling. Mast cells (MCs), key immune effector cells capable of rapid mediator release through degranulation, also express TRPV4. Increasing evidence supports TRPV4-MC signaling as an important neuroimmune interface, linking mechanical and inflammatory stimuli to tissue hypersensitivity and pain. In this review, we synthesize current evidence supporting a role for TRPV4 in MC-associated neuroimmune signaling across multiple disease contexts while distinguishing settings in which TRPV4 directly regulates MC activation from those in which MC responses arise through multicellular tissue interactions. Direct TRPV4-dependent MC activation has been described in conditions such as LL-37–driven rosacea and mechanically induced inflammation, whereas in disorders including asthma, visceral hypersensitivity, bladder pain syndromes, and osteoarthritis, TRPV4 activity in epithelial, neuronal, or stromal compartments more often influences MC function indirectly through ATP–purinergic signaling, cytokine release, and neuropeptide-mediated crosstalk. Across systems, TRPV4 emerges not as a single pathogenic switch but as part of a context-dependent signaling network whose functional consequences depend on cell type, tissue microenvironment, and disease stage. Altogether, these findings identify TRPV4 as a therapeutically actionable node within neuroimmune signaling pathways and support the development of tissue-specific and combination strategies targeting both TRPV4 activity and MC-mediated signaling in chronic inflammatory and pain disorders. Full article

Eosinophils are multifunctional granulocytes with central roles in the pathobiology of chronic airway diseases. While systemic eosinophilia (>300 cells/μL) is a well-established biomarker to guide therapeutic decision-making, accumulating evidence indicates that eosinophils are not a uniform population but instead exhibit substantial phenotypic and functional heterogeneity across biological compartments, inflammatory states, and disease contexts. In this review, we synthesize the current understanding of eosinophil heterogeneity in airway diseases and critically evaluate the strengths and limitations of surface marker-based approaches, with emphasis on CD62L/L-selectin-defined subpopulations. Although CD62L-based stratification has provided valuable insight into eosinophil activation and tissue localization, its limited specificity, inconsistent clinical associations, and reliance on murine models restrict its utility as a framework for eosinophil subtyping in humans. We highlight how transcriptomic and proteomic profiling has transformed the field by revealing that peripheral blood eosinophils are largely quiescent, whereas disease-relevant functional specialization is predominantly acquired within inflamed tissues in response to cues from the local microenvironment. These molecular studies support a model in which eosinophil heterogeneity represents a continuum of activation rather than discrete, fixed subsets. A refined, integrative approach to understanding eosinophil heterogeneity is critical for improving patient stratification, predicting therapeutic responsiveness, and optimizing precision medicine strategies in chronic airway diseases. Full article

We assess associations between emergency room (ER) visits, scaled to per 10⁵ population per year, for asthma and chronic obstructive pulmonary disease (COPD), two of the most common respiratory diseases, and zip code-level exposure to criteria air pollutants (CAPs) coming from point sources in New York State (NYS) from 2010 to 2018. Exposure data on point source CAPs were retrieved from the United States Environmental Protection Agency (USEPA) National Emission Inventory (NEI) database, and ER visits for asthma and COPD were acquired from the New York State Department of Health (NYSDOH) Statewide Planning and Research Cooperative System (SPARCS). To account for within-county variability, we used log-linear mixed effects models, adjusted for year, sex, age category, county-level poverty, smoking, PM_2.5, volatile organic compounds (VOCs), and CAPs sources within the study period. Results show significant associations between ER visits for asthma and COPD and most of the pollutants in the study, even after adjusting for the effects of poverty and smoking. Although point source emissions comprise a small portion of total air pollution, our findings show that zip code-level point source CAPs, especially the gaseous pollutants, pose a modest but significant contribution to the risk of respiratory disease-related ER visits. Full article

In the body, mast cells are found in circulation and located in tissues. These immune cells arise in the bone marrow and are often associated with conditions such as allergies and asthma. However, these cells also play roles in other inflammatory reactions, dysregulated wound healing and chronic conditions. Regarding their presence in tissues of the intervertebral disc (IVD), mast cells have been located in the normal nucleus pulposus, and reports indicate mast cell numbers are elevated in IVD degenerative conditions. As the integrity of the IVD is reported to decline with ageing as well as in sciatica and clinically defined degenerative conditions, targeting mast cell function may be a viable conservative treatment option for the ageing IVD in health and disease. This review discusses the possible involvement of mast cells in IVD health and disease, and the rationale for the use of mast cell stabilizers such as ketotifen as potential treatment options for conditions affecting IVD integrity. Such mast cell targeting treatments may be considered alone or in combination with other molecules such as specific proteinase inhibitors impacting proteinases known to be present in the affected tissues, such as MMP-3 and HTRA1. Thus, a multicomponent approach in such treatments may provide effectiveness in inhibiting progressive loss of IVD integrity and function in chronic degenerative conditions or adverse outcomes due to non-resorption of extruded nucleus pulposus in sciatica. Full article

Background/Objectives: Obstructive sleep apnea (OSA) syndrome is characterized by recurrent upper airway obstruction during sleep and is closely associated with systemic inflammation and cardiometabolic risk. α-Klotho and fibroblast growth factor-23 (FGF-23) are emerging biomarkers with potential roles in vascular homeostasis, inflammation, and metabolic regulation. However, their relevance in OSA remains insufficiently elucidated. The aim of this study was to evaluate serum α-Klotho and FGF-23 levels in patients with OSA and to investigate their associations with disease severity. This represents a novel approach that may provide new insights into the pathophysiological mechanisms linking OSA with cardiometabolic risk. Methods: A total of 133 participants were included in this study and categorized into three groups according to apnea–hypopnea index: 1—simple snoring (n = 44); 2—non-severe OSA (n = 44); and 3—severe OSA (n = 45). Comparisons between two groups were performed using Student’s t-test for normally distributed variables. Comparisons among three or more groups were conducted using one-way ANOVA and the Kruskal–Wallis test. ANCOVA was applied to compare α-Klotho and FGF-23 levels between groups after adjustment for age, BMI, diabetes, hypertension, asthma, COPD, and thyroid disease. The predictive performance of α-Klotho and FGF-23 for severe obstructive sleep apnea was evaluated using ROC curve analysis. Results: Serum α-Klotho levels decreased significantly with increasing OSA severity (p = 0.001). Serum FGF-23 levels increased significantly across AHI groups (p = 0.001). After adjustment for age, BMI, diabetes, hypertension, asthma, thyroid disease, COPD and vitamin D levels, α-Klotho levels were lower in the severe and non-severe OSA group (p = 0.001, both) compared to the simple snoring group, whereas FGF-23 levels were higher in the severe and non-severe OSA group (p = 0.001; both) compared to the simple snoring group. In predicting the risk of severe OSA compared with non-severe OSA, an α-Klotho cut-off value of 280.3 yielded a sensitivity of 84.44% and specificity of 75%, whereas an FGF-23 cut-off value of 75.5 yielded a sensitivity of 62.2% and specificity of 72.7%. Conclusions: Serum α-Klotho levels significantly decrease while FGF-23 levels increase in correlation with OSA severity. α-Klotho exhibited superior predictive performance over FGF-23 in identifying severe OSA, suggesting its potential as a more sensitive biomarker for systemic involvement. These results indicate that the α-Klotho/FGF-23 axis is independently associated with OSA and may play a pivotal role in the pathophysiological mechanisms linking intermittent hypoxia to increased cardiometabolic risk. Full article

Background: Tezepelumab has demonstrated efficacy in severe uncontrolled asthma (SUA), although real-world evidence remains limited. Methods: We included patients with SUA who completed at least 6 months of treatment. Lung function, eosinophil counts, IgE, FeNO, comorbidities, and changes in asthma control were assessed using ACT, ACQ, the VAS, and quality of life (AQLQ), as well as severe exacerbations (hospital admissions and emergency visits), oral corticosteroid (OCS) courses, OCS withdrawal/dose reduction, and reductions in maintenance and reliever medication. Response was evaluated using the FEOS and EXACTO scales. Baseline (T0) and 6-month (T6) outcomes were compared in the overall cohort and according to T2-high (eosinophilic/allergic) vs. T2-low phenotype. Results: A total of 33 patients were analyzed (58 ± 12 years; 94% women), with a high burden of comorbidities (88%), mainly rhinosinusitis (79%), obesity (41%), and smoking (37%). Of these, 45.5% had received prior biologic therapy. All patients were on high-dose ICS + LABA, frequently with LAMA and other controllers; 30% were on maintenance OCS. In the previous year, 49% had been hospitalized, 97% had attended the emergency department, and 100% required OCS courses. After 10 ± 3 months, the overall group showed significant improvement in VAS, ACT, ACQ, and AQLQ (p < 0.001), with a reduction in eosinophils, but no significant change in FEV1%. Severe exacerbations, emergency visits, hospitalizations, and OCS courses decreased markedly (p < 0.001). Among 10 patients on maintenance OCS, OCS were discontinued in 7 and reduced in 3; maintenance/reliever medication was also reduced. The T2-high phenotype showed a higher likelihood of “complete response” (52% vs. 17% in non-T2), although “good response” predominated in non-T2; this difference was significant (p = 0.04). Conclusions: Tezepelumab improved asthma control and reduced healthcare utilization and corticosteroid use in both T2 and non-T2 patients, achieving clinical remission in 40%, with better outcomes in T2. Full article

The genus Psiadia (Asteraceae), widely distributed in Madagascar and the Mascarene Islands (Mauritius, La Réunion, Rodrigues), is traditionally used to treat bronchitis, asthma, colds, abdominal pain, and other inflammatory disorders. However, few studies have scientifically validated these traditional medicinal uses. To assess P. dentata as a valuable source of bioactive natural products, a combined ¹H NMR-based metabolomic, molecular networking, and phytochemical study was conducted. Multivariate analysis (PLS-DA) of crude extracts from Psiadia species collected on Reunion Island enabled rapid discrimination of active extracts from P. dentata and revealed two methoxylated flavonoids and one coumarin as metabolites correlated with its antiplasmodial and anti-inflammatory activities. Additionally, UHPLC-DAD-ESI-QTOF-MS/MS molecular networking approach enabled detailed chemical profiling of this species, allowing the annotation of 25 compounds (1–25) in this species. Subsequent phytochemical investigation of P. dentata leaves led to the isolation and identification of 25 metabolites, including nine new diterpenes (26–34), one new coumarin (35), and 15 known compounds (1–8, 11, 18, 19 and 36–39) from the diterpenoid, flavonoid, and coumarin families. The structures of the new compounds were elucidated using spectroscopic methods, including extensive 1D and 2D NMR and HRESIMS analyses. Biological evaluation of the isolated compounds showed that compounds 1, 7, 26 and 27 showed antiplasmodial activity against Plasmodium falciparum (3D7 strain, IC₅₀ = 7.25–13.46 μM). Compounds 7, 26, 27, 31 and 32 inhibited nitric oxide production (IC₅₀ = 0.87–27.71 μM), indicating potential anti-inflammatory effects. Only compound 1 displayed moderate cytotoxicity against HepG2 and HT29 cancer cell lines (IC₅₀ = 25.67 and 18.35 μM, respectively). Full article

Background and Objectives: Emphysema and coronary artery calcium (CAC) share common lifestyle-related risk factors, yet their association in Chinese populations remains understudied. This study investigated how lifestyle factors influence the association between emphysema and CAC score in an urban Chinese general population. Methods: The study included 1000 participants from the Chinese Nelcin-B3 urban general population study originating in 2017 who underwent low-dose CT (LDCT) screening and comprehensive CT assessment. Emphysema was visually assessed by subtype and severity. CAC was measured using the Agatston method and categorized as 0, 1–100, and >100. Questionnaire-based lifestyle factors (smoking, BMI, diet, physical activity, alcohol consumption and environmental exposures) were categorized based on number of unfavorable behaviors. Multivariable multinomial logistic regression adjusted for age, sex, education and cardiovascular risk factors examined the associations between emphysema and CAC, with interactions and stratified analyses for lifestyle effects. Results: Emphysema was present in 62.3% of the participants, with centrilobular being the most common subtype (61.5%). Paraseptal emphysema was associated with both CAC 1–100 (OR: 2.07 [1.03–4.15]) and CAC > 100 (OR: 2.94 [1.26–6.84]). Severe emphysema was linked to CAC > 100 (OR: 3.50 [1.38–8.84]). These associations were stronger in the intermediate unhealthy lifestyle group for paraseptal (OR: 5.41 [1.70–17.22] and moderate and severe emphysema (OR: 9.64 [1.64–56.55]; OR: 3.73 [1.07–13.06]), respectively, but not significantly different. Conclusions: While paraseptal and severe emphysema are associated with higher CAC scores, there is no modifying effect of lifestyle factors. These findings suggest that cardiovascular risk assessment could be of importance in individuals with emphysema. Further longitudinal studies are needed to clarify the clinical implications. Full article