Asthma is a common chronic respiratory condition that significantly affects the quality of life, academic performance, and mental health of college students. Among those living in hostels, these challenges are often amplified by environmental triggers such as poor ventilation, dampness, mold, and temperature-related conditions, as well as psychosocial stressors linked to communal living. This perspective explores the overlooked intersection between asthma management, mental well-being, and institutional responsibility within hostel settings. It discusses how corticosteroid therapy, while essential for disease control, may contribute to psychiatric symptoms that further complicate adherence and daily functioning. Many students experience stigma, embarrassment about inhaler use, and inadequate support from hostel staff during exacerbations, which collectively lead to poor control and academic decline. Addressing these issues demands a shift beyond pharmacological approaches toward comprehensive institutional strategies that include environmental assessment and remediation, appropriate indoor temperature and humidity control, routine medical screening, staff training, peer support, and digital self-management tools. By fostering awareness and integrating psychosocial support into campus health systems, colleges can create safer and more inclusive environments for students with asthma, ultimately improving both respiratory outcomes and overall well-being.
BACKGROUND:Asthma control remains suboptimal in a large proportion of patients, partly due to poor treatment adherence. Illness and treatment perceptions have been identified as key determinants of adherence and disease outcomes; however, their combined influence has been less frequently examined using person-centered approaches. OBJECTIVE:To identify latent profiles of illness perceptions, treatment beliefs and adherence behaviors in Mexican adults with asthma, and to examine differences in asthma control across these profiles. METHODS:A cross-sectional study was conducted with 264 adults with asthma. Latent profile analysis was performed using indicators of illness perceptions, treatment beliefs and adherence behaviors. Models were compared using AIC, BIC, entropy, BLRT and class size. Between-profile differences in asthma control and clinical variables were examined using nonparametric tests in R. RESULTS:A three-profile solution was selected. Profile 1 showed intermediate levels across most indicators. Profile 2 was characterized by higher emotional representations, perceived consequences and treatment concerns, as well as lower illness coherence and lower adherence, and was associated with poorer asthma control. Profile 3 showed lower emotional burden, higher illness understanding, greater personal control, higher adherence and better asthma control. Significant differences were observed across profiles in asthma control, rescue inhaler use and emergency department visits, although effect sizes for clinical outcomes were small. CONCLUSIONS:Distinct profiles were associated with differences in asthma control. Emotional representations and treatment concerns appear to play a central role in identifying patients at higher risk of poor adherence and suboptimal asthma control. These findings support the relevance of incorporating psychological assessment into asthma management and tailoring interventions according to patient profiles.
To evaluate the associations of multidimensional atmospheric humidity indicators and air pollution with self-reported chronic lung disease (CLD) among middle-aged and older adults in China. METHODS:Data from 16,204 adults aged ≥45 years from the 2011, 2013, and 2015 waves of the China Health and Retirement Longitudinal Study (CHARLS) were analyzed. Annual exposures to six air pollutants (CO, NO₂, O₃, PM₂.₅, PM₁。, SO₂) and six humidity indicators (RH, AVP, VPD, DPT, MR, SH) were estimated at 1-km resolution. Multivariable logistic regression and restricted cubic spline models were applied. Stratified and sensitivity analyses were conducted. RESULTS:Higher concentrations of CO, NO₂, O₃, PM₂.₅, and SO₂ were linearly associated with increased self-reported CLD risk, while PM₁。 showed an approximate U-shaped relationship. Each interquartile-range increase in air pollutant concentrations was associated with an 18-45% higher odds of self-reported CLD. AVP, VPD, DPT, MR, and SH were positively associated with self-reported CLD risk, whereas RH exhibited an inverted U-shaped pattern. Weighted quantile sum analyses showed significant positive associations for both air pollution and humidity mixtures. A significant interaction between RH and sex was observed. Sensitivity analyses across different lag structures confirmed that air pollutants and atmospheric humidity were consistently associated with self-reported CLD risk. CONCLUSIONS:Long-term exposure to ambient air pollution and multidimensional humidity indicators was independently associated with higher self-reported CLD risk, highlighting the importance of considering meteorological factors in disease prevention.
In children aged 6-11 years with persistent asthma, earlier use of inhaled corticosteroid (ICS)-long-acting beta-2 agonist combination therapies has become a topic of increasing interest in recent years; however, available evidence in this age group remains limited. This study aimed to compare ICS monotherapy, fixed-dose ICS/salmeterol, and fixed-dose ICS/formoterol therapies regarding asthma exacerbations requiring systemic corticosteroids. METHODS:This retrospective study included children aged 6-11 years with persistent asthma who were followed for at least 1 year while receiving regular inhaled therapy between January 2021 and August 2024. Patients classified as The Global Initiative for Asthma (GINA) steps 2-4 were grouped according to treatment with ICS monotherapy, fixed-dose ICS/salmeterol, or fixed-dose ICS/formoterol. Asthma exacerbations were assessed based on the need for systemic corticosteroids, emergency department visits, and/or hospitalization. RESULTS:A total of 296 children aged 6-11 years with persistent asthma met the inclusion criteria: 184 received fluticasone propionate (FP), 47 received fluticasone propionate/salmeterol (FP/SAL), and 65 received budesonide/formoterol (BUD/FOR). The groups differed in age at initiation of inhaled therapy (p < 0.001) and duration of follow-up (p = 0.014). Overall, 113 patients (38.2%) experienced at least one asthma exacerbation during follow-up, with no significant difference among FP, FP/SAL, and BUD/FOR groups (p = 0.93). Rates of emergency department visits and hospital admissions were also comparable between groups (p = 0.805 and p = 0.383, respectively), and no significant differences were found regarding systemic corticosteroid-requiring asthma exacerbations. CONCLUSIONS:In children aged 6-11 years with persistent asthma, no single controller therapy demonstrated clear superiority in preventing asthma exacerbations.
OBJECTIVE:To provide a clinically grounded and pathobiological review of eosinophilic inflammation in severe asthma, addressing mechanisms, diagnostic interpretation, and implications for biologic therapy selection. METHODS:Narrative review of guidelines, pivotal phase 2-3 randomized controlled trials, meta-analyses, registry data, and key translational studies evaluating eosinophils, type 2 (T2) inflammation, and targeted biologic therapies in severe asthma and eosinophilic chronic obstructive pulmonary disease. Publications were selected based on clinical relevance, methodological rigor, and impact on contemporary severe asthma management. Evidence was critically appraised and integrated with expert clinical perspective. No predefined systematic protocol or formal risk-of-bias assessment was undertaken. RESULTS:Eosinophils are central effector cells in T2-high severe asthma, contributing to airway inflammation, epithelial injury, mucus plugging, and remodeling. Interleukin (IL)-5 is the principal regulator of eosinophil maturation and survival, while IL-4, IL-13, and epithelial alarmins modulate tissue recruitment and amplification of inflammation. Blood eosinophil count (BEC) remains the most accessible biomarker in practice; however, its interpretation requires contextualization, considering corticosteroid exposure, biological variability, age at onset, and comorbidities. No single biomarker fully reflects airway eosinophilia, supporting a multidimensional assessment integrating clinical phenotype, longitudinal biomarkers, imaging, lung function, and therapeutic response. Biologics have transformed outcomes, with greater efficacy generally observed at higher BEC levels. CONCLUSION:Eosinophilia should be interpreted as a contextual biomarker within a comprehensive clinical framework. Precision phenotyping is essential to optimize biologic selection and advance toward sustained disease control and clinical remission in severe asthma.
OBJECTIVE:To evaluate current evidence on airway and gut microbiome alterations in asthma pathogenesis, inflammatory heterogeneity, and therapeutic response, and to examine microbiome-targeted interventions and artificial intelligence (AI)-based approaches for precision asthma medicine. METHODS:A structured narrative review was conducted using PubMed, Scopus, and Google Scholar to identify key literature published from 2015 to 2026, supplemented by landmark studies where appropriate. The review focused on microbiome dysbiosis, host-microbe interactions, inflammatory endotypes, microbiome-targeted interventions, biologic therapies, and AI- and machine-learning-based approaches relevant to precision asthma care. RESULTS:Asthma-associated microbiome alterations were linked to disease heterogeneity, inflammatory endotypes, exacerbation risk, and treatment response, although evidence remained largely associative. Airway dysbiosis, particularly enrichment of Haemophilus, Moraxella, and Neisseria, was associated with neutrophilic inflammation and exacerbation-prone disease. Gut microbiota and short-chain fatty acid-producing bacteria were implicated in immune regulation through the gut-lung axis. Probiotics, prebiotics, synbiotics, postbiotics, engineered microbial consortia, and bacteriophages showed promise but remain investigational. Biologics targeting IgE, IL-5/IL-5R, IL-4Rα, and TSLP improved outcomes in selected patients, but microbiome-based response predictors remain unvalidated. AI/ML integrating microbiome, multi-omic, clinical, and environmental data showed potential for endotype classification, exacerbation prediction, biomarker discovery, and treatment-response prediction, but require robust validation. CONCLUSION:The airway and gut microbiomes offer promising biomarkers and therapeutic targets for precision asthma care. Integration of multi-omic, clinical, and environmental data with AI may improve patient stratification and therapeutic decision-making, but standardized methodologies and large prospective, multicenter, externally validated studies are needed before routine clinical implementation.
OBJECTIVE:Body Roundness Index (BRI) is a new measure of central fat distribution linked to asthma risks, but its connection to asthma in children is unclear. This study investigates the relationship between BRI and asthma in U.S. children and adolescents. METHODS:We conducted a cross-sectional study of 32,738 participants aged 3-17 years using National Health and Nutrition Examination Survey (NHANES) data (1999-2023). BRI was calculated from height and waist, and logistic regression estimated the BRI-asthma association, adjusting for age, sex, race/ethnicity, education level, poverty income ratio, physical activity, and passive smoking (serum cotinine). RESULTS:In the study population, 5609 (17.13%) had asthma. A nonlinear association was observed between BRI and asthma. We identified a critical BRI threshold value of approximately 3.59. For BRI values below 3.59, each unit increase in BRI was associated with higher odds of asthma (OR = 1.25, 95% confidence interval (CI): 1.18-1.32, p < 0.001). In contrast, for BRI values above 3.59, the increase in odds was more modest, yet remained significant (OR = 1.06, 95% CI: 1.02-1.09, p = 0.001). A log-likelihood ratio test confirmed the nonlinear association (p < 0.001). CONCLUSIONS:In this study of U.S. children and adolescents, a higher BRI was associated with a greater risk of having asthma. The relationship was nonlinear, with a pronounced increase in asthma risk at lower BRI levels, while the increase leveled off at higher levels. Given the cross-sectional design, causality cannot be inferred.
BACKGROUND:Pentraxin-3 (PTX-3) is a humoral pattern recognition receptor involved in innate immunity and inflammation regulation, but its relationship with lung function remains unclear. OBJECTIVE:This study investigated the association between serum PTX-3 levels and respiratory function in preschool wheezy children (CW), considering wheezing phenotypes and atopy. METHODS:In this cohort study, 165 preschoolers were divided into 84 wheezy children (CW) and 81 healthy controls (HC). Serum PTX-3 levels, eosinophil counts, and pulmonary function using impulse oscillometry (IOS) were assessed. IOS parameters included zR5, zR20, R5-20, zX5, zX20, Fres, and AX. Comparisons were made according to wheezing phenotype (multi-trigger vs episodic) and atopy status. Correlation analysis between PTX-3 and IOS parameters was performed. RESULTS:The CW group had higher PTX-3 levels (p = 0.010), increased IOS parameters (zR5, zR20, R5-20, Fres, AX; p < 0.05), and reduced zX5 (p < 0.001). PTX-3 positively correlated with zR5, zR20, and AX (r:0.220-0.226, p < 0.05). Multi-trigger wheezing and atopy were associated with higher R5-20 and PTX-3 (p < 0.05). Children with parental atopy also showed higher PTX-3 and airway resistance. CONCLUSION:Elevated PTX-3 is associated with impaired lung function in preschool wheezy children and may serve as a biomarker for respiratory function, phenotype differentiation, and atopy.
OBJECTIVE:Parental numeracy skills, reflecting a quantitative domain within health literacy, may be relevant to pediatric asthma management. However, the association between parental numeracy skills and the asthma-related quality of life (QOL) of children with asthma remains insufficiently examined. This study aimed to assess the QOL of Jordanian children with asthma and to examine its association with parental numeracy skills. METHODS:A cross-sectional study was performed on a sample of 400 parents (66.5% mothers) of children with asthma (59.5% male) undergoing treatment at the University of Jordan Hospital. The Arabic version of the Asthma Numeracy Questionnaire (Ar-ANQ) was utilized to evaluate parental numeracy skills, while the parent-report version of the Pediatric Quality of Life Inventory (PedsQL) Asthma Module was employed to assess QOL. Quantile regression analyzed associations between parental numeracy skills, asthma control, and QOL. RESULTS:The median Ar-ANQ score was 3 (IQR: 1-4) out of 4, and the median QOL score was 60 (IQR: 50-67) out of 100. Higher parental numeracy skills were significantly associated with better asthma-related QOL among children (β = 1.99, 95% CI [0.81, 3.18], p = 0.001). Children with uncontrolled or partially controlled asthma had significantly lower QOL scores (β = -9.70, 95% CI [-15.57, -3.82], p = 0.001; β = -10.06, 95% CI [-15.83, -4.29], p = 0.001). CONCLUSIONS:Higher parental numeracy skills were associated with better asthma-related QOL among children with asthma. Given the cross-sectional design, this finding should be interpreted as an association rather than evidence of a causal effect.
OBJECTIVES:a key feature of asthma is airway hyperresponsiveness (AHR), which is typically diagnosed through methacholine challenge testing (MCT). Fractional exhaled nitric oxide (FENO) is a noninvasive marker of type-2 inflammation. Extended nitric oxide analysis breaks this down into bronchial (JawNO) and alveolar (CANO) components; we aimed to determine whether this extensive analysis offers added value in diagnosing AHR beyond what conventional FENO testing can provide. METHODS:seventy-two consecutive patients referred for MCT were prospectively enrolled and underwent spirometry, extended nitric oxide analysis, and MCT. AHR was defined using three methacholine dose thresholds for PD20FEV1 (≤400, ≤800, and ≤1600 µg). RESULTS:AHR prevalence ranged from 23.6% at the lowest threshold (≤400 µg) to 44.4% at the highest (≤1600 µg). Patients with positive AHR had significantly elevated FENO and JawNO across all thresholds. The best FENO and JawNO cutoffs provided strong negative predictive values, but their positive predictive values were low. CONCLUSION:extended nitric oxide analysis-especially FENO and JawNO-may improves the diagnostic capability of exhaled nitric oxide in predicting AHR. These findings highlight its potential as a quick, noninvasive way to rule out AHR, which could simplify asthma diagnosis and reduce the need for lengthy bronchial challenge testing.
OBJECTIVE:To evaluate whether montelukast combined with inhaled corticosteroids (ICS) increases the risk of neuropsychiatric adverse events (NEs) compared with ICS monotherapy in pediatric and adolescent asthma patients. METHODS:A systematic review and meta-analysis was conducted according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines (PROSPERO registration: CRD420251070948). PubMed, Cochrane Library, Embase, Web of Science, and ClinicalTrials.gov were searched for studies comparing montelukast plus ICS with ICS alone. The primary outcome was the occurrence of NEs. RESULTS:Six studies (three randomized controlled trials and three cohort studies) involving 559 pediatric patients were included. The incidence of NEs was 12.1% in the montelukast plus ICS group and 8.6% in the ICS-only group. The pooled risk ratio was 1.41 (95% CI: 0.89-2.22; p = 0.14), with an absolute risk difference of 3.5% (95% CI: -1.2% to 8.2%). This corresponded to approximately 35 additional events per 1000 children (95% CI: -12 to 82). Sensitivity analyses and risk-of-bias assessments supported the robustness of the findings. Subgroup analyses suggested possible increases in headache and sleep disturbances, although these differences were not statistically significant. CONCLUSIONS:Montelukast combined with ICS may be associated with an increased risk of NEs in pediatric asthma patients; however, the current evidence remains uncertain. Clinicians should consider potential neuropsychiatric risks when prescribing combination therapy, particularly for susceptible children. Further prospective studies are warranted to confirm these findings.
OBJECTIVE:To evaluate the safety and clinical improvements with once daily fixed dose combination (FDC) of montelukast 10 mg and acebrophylline sustained-release 200 mg tablet in patients with asthma. METHODS:This multicenter, single-arm, open-label, prospective, phase IV clinical trial included adult patients with moderate to severe asthma. Patients meeting eligibility criteria based on GINA guidelines were included. They underwent a washout before initiating the 12-week treatment. Study visits included screening and enrollment visits, and follow-ups on days 28, 56, and 84.The primary outcome was the incidence of adverse events (AEs), while secondary outcomes included changes in trough forced expiratory volume in one second (FEV1), forced vital capacity (FVC), Asthma Symptom Utility Index (ASUI) scores, and rescue medication use. RESULTS:A total of 211 patients with asthma were included. The mean ± SD age and body mass index (BMI) were 39.52 ± 11.68 years and 23.83 ± 4.37 kg/m2, respectively. AEs were reported in 10.9% of patients, and most AEs were of mild severity. One serious AE, unrelated to treatment, resulted in treatment withdrawal. Lung function showed significant improvement, with mean changes from baseline to Day 84 of 0.61 ± 0.56 L in FEV1, 0.51 ± 0.65 L in FVC, and 0.17 ± 0.14 in ASUI scores (p < 0.0001 for all). Rescue medication use decreased progressively, with fewer patients requiring it by Day 84. CONCLUSION:The findings demonstrate that the FDC of montelukast and acebrophylline has a favorable safety profile and is associated with improvements in lung function and asthma symptoms. TRIAL REGISTRATION:CTRI/2020/02/023237 [Registered on: 11/02/2020] Trial Registered Prospectively, URL: https://ctri.nic.in/Clinicaltrials/pmaindet2.php?EncHid=MzY1MjU=&Enc=&userName=.
OBJECTIVE:This retrospective diagnostic test aimed to explore a method that can differentiate asthma from COPD with incomplete reversible airflow limitation. METHODS:Patients diagnosed with asthma and COPD from June 19, 2024, to November 16, 2025, were enrolled as training samples. Intergroup data were analyzed through discriminant analysis to determine the quantitative diagnostic formula and the discriminant boundary value Zc that could identify them. A portion of the patients collected in the same way were used as validation samples to verify the accuracy of the model. RESULTS:128 patients with asthma and 142 with COPD were enrolled as training samples. Through discriminant analysis, the quantitative diagnostic formula was Zi = 1.476X1+0.348X2-0.269X3-0.465X4+0.995X5+0.046X6+0.013X7-4.479 (X1 = 0 and X1 = 1 represent the absence or presence of the concave pattern in the F-V, respectively; X2, X3 and X4 represent forced vital capacity, forced expiratory volume in 1s, and peak expiratory flow, as indicators of bronchodilation test, respectively, 0 = negative, 1 = positive; X5 represents gender, X5 = 0 indicates female, and X5 = 1 indicates male; X6 represents age; X7 represents smoking index), and Zc = -0.0687. The accuracy of the quantitative diagnostic formula, validated internally and externally using 121 patients, was 90.40% and 87.60%, respectively. CONCLUSIONS:The multimodal respiratory function diagnostic model, utilizing discriminant analysis, can distinguish asthma with incomplete reversible airflow limitation from COPD when the strongest expiratory effort is performed with an extrapolated volume ≤0.10 L.
OBJECTIVE:To characterize the burden and temporal trends of asthma estimated as attributable to high body mass index (BMI) among children aged 0-14 years using Global Burden of Disease (GBD) 2021 estimates, with analyses by location, sociodemographic level, sex, and age, and to project trends through 2050. METHODS:Using modeled GBD 2021 estimates, we conducted a descriptive analysis of high BMI-attributable asthma among children aged 0-14 years from 1990 to 2021. Outcomes included deaths, disability-adjusted life years (DALYs), age-standardized mortality rate (ASMR), and age-standardized DALY rate (ASDR). Temporal trends were assessed using estimated annual percentage change (EAPC), Joinpoint regression, and autoregressive integrated moving average (ARIMA) forecasts to 2050. RESULTS:Globally, ASDR increased from 14.43 to 17.09 per 100,000 (EAPC 0.67), while ASMR declined from 0.036 to 0.021 per 100,000 (EAPC -1.66). Mortality was concentrated among children younger than five years, while disability increased mainly in the 5-9 and 10-14 age groups after 2009. The fastest ASMR declines occurred in high-income Asia Pacific and East Asia, whereas ASDR increased in high and high-middle Socio-demographic Index (SDI) settings. ARIMA models projected continued decline in ASMR to 0.004 and increased ASDR to 21 per 100,000 by 2050. CONCLUSIONS:From 1990 to 2021, modeled population-level estimates showed declining mortality but increasing disability burden for high BMI-attributable pediatric asthma, with marked regional and SDI disparities. ARIMA forecasts suggested that mortality may continue to decline, whereas disability burden may further increase through 2050.
BACKGROUND:Cough variant asthma (CVA) in children frequently precedes typical asthma (TA), yet accurate prediction of this progression remains challenging. METHODS:A prospective cohort of 289 children diagnosed with CVA between June 2023 and June 2024 was followed for 12 months until June 2025. Patients were randomly divided into a training set (n = 203) and a validation set (n = 86) in a 7:3 ratio. Predictors were screened by univariate logistic regression and LASSO regression. A nomogram was constructed using the rms package in R and evaluated by ROC curves, 1000-iteration Bootstrap calibration, decision curve analysis (DCA), and Hosmer-Lemeshow tests. RESULTS:During the 12-month follow-up, 42 children (14.5%) progressed to TA. Ten independent predictors were finally selected by LASSO regression and incorporated into the nomogram: personal history of allergy (OR = 3.62, 95% CI:1.78-7.36), family history of asthma (OR = 3.18, 95% CI:1.37-7.39), poor treatment compliance (OR = 2.94, 95% CI:1.32-6.55), history of pet keeping (OR = 2.41, 95% CI: 1.11-5.24), FeNO (OR = 1.09, 95% CI:1.05-1.14), CaNO (OR = 1.16, 95% CI: 1.06-1.27), X5%pred (OR = 1.04, 95% CI:1.02-1.07), R5%pred (OR = 1.03, 95% CI:1.01-1.06), FEF25%pred (OR = 0.96, 95% CI:0.94-0.98), and MMEF%pred (OR = 0.97, 95% CI: 0.95-0.99). The nomogram showed good discrimination with AUCs of 0.863 (95% CI: 0.782-0.944) in the training set and 0.838 (95% CI:0.742-0.933) in the validation set. Hosmer-Lemeshow tests indicated good fit (training:χ2=6.7277, P = 0.5663; validation:χ2=7.7376, P = 0.4595). DCA demonstrated favourable clinical net benefit across a wide range of threshold probabilities. CONCLUSIONS:This novel nomogram integrating ten key risk factors provides a preliminary and visually intuitive tool for risk stratification of CVA progression to TA in children.
OBJECTIVE:This study investigated the clinical significance of miR-431-5p in childhood asthma and its cell function in house dust mite (HDM)-induced cell models. METHODS:Differential miRNA expression was analyzed in the GSE263408 dataset using bioinformatics tools (Limma package). Serum levels of miR-431-5p and CD34 mRNA in asthmatic and healthy children were measured. The diagnostic and prognostic potentials of miR-431-5p were evaluated using ROC curve analysis. The targeting relationship between miR-431-5p and CD34 was predicted by TargetScan and validated by dual-luciferase reporter assay. In vitro, transfected with miR-431-5p mimic or CD34 pcDNA, human airway smooth muscle cells (ASMCs) and mast cells were treated with HDM to assess effects on RNA expression, ASMC cell viability, and mast cell degranulation/histamine content. RESULTS:Bioinformatic analysis identified miR-431-5p as differentially expressed in asthma. Serum miR-431-5p was significantly downregulated in asthmatic children compared to healthy controls, showing diagnostic value (AUC = 0.866). It was further decreased in children with asthma recurrence/exacerbation, with an AUC of 0.787 in discriminating recurrence/exacerbation from none. miR-431-5p targeted CD34 3'UTR. In HDM-induced ASMCs, miR-431-5p mimic reduced CD34, MUC5AC mRNA, and cell viability, which were rescued by CD34 overexpression. In HDM-induced mast cells, miR-431-5p mimic reduced CD34 mRNA, degranulation, and histamine content, effects also reversed by CD34 overexpression. CONCLUSIONS:Serum miR-431-5p has potential as a biomarker for childhood asthma. miR-431-5p may mitigate asthma-related cellular processes by targeting CD34.
Objective: Childhood allergic asthma (CAA) is a chronic allergen-driven airway inflammatory disease whose molecular mechanisms and precise diagnostic and therapeutic strategies remain incompletely understood. This study aimed to identify mitochondrial-mitophagy-related genes (MMRGs) with diagnostic and therapeutic potential in CAA.Methods: Public transcriptomic datasets were analyzed using weighted gene co-expression network analysis and multiple machine learning algorithms to identify diagnostic signature genes and construct a CAA diagnostic model. Immune infiltration, competing endogenous RNA network, and drug-gene interaction analyses were subsequently performed. The expression and biological functions of selected genes were further evaluated in an IL-13-stimulated airway epithelial cell model.Results: Fifteen MMRG-related signature genes with diagnostic potential were identified, and the resulting diagnostic model exhibited good predictive performance. Several immune cell subsets, including resting mast cells, and naive B cells, showed altered infiltration in CAA, and their abundances were significantly correlated with signature-gene expression. The constructed ceRNA network indicated complex post-transcriptional regulation of these genes. Drug-gene interaction analysis identified multiple potential therapeutic compounds, with BCL2-related agents being the most abundant. In IL-13-stimulated airway epithelial cells, MRPL43 expression was increased, whereas BCL2 expression was decreased. MRPL43 knockdown significantly restored cell viability and reduced the secretion of pro-inflammatory cytokines.Conclusions: MMRGs are closely associated with the diagnosis, immune microenvironment, and potential therapeutic regulation of CAA. MRPL43 may contribute to airway epithelial inflammation and represents a potential biomarker and therapeutic target for CAA.
