Search Results (1,461)

Catheter ablation is the cornerstone of rhythm control in atrial fibrillation (AF), yet recurrence remains common, and obesity is among the most consistently implicated modifiable risk factors. Weight reduction and metabolic pharmacotherapy are increasingly used in the periprocedural period, but whether they act through a shared pathway has not been systematically examined. This narrative review compares the two approaches and asks whether metabolic agents confer protection beyond weight loss itself. Three observations argue that they do not act identically. First, the benefit of weight reduction is dose-dependent yet contingent on delivery: a structured, physician-led risk-factor program reduced 12-month arrhythmia recurrence (risk ratio 0.53), whereas nurse-led care that improved guideline adherence without structured delivery did not alter the primary endpoint. Second, sodium-glucose cotransporter 2 inhibitors (SGLT2i) have been associated with reduced recurrence across BMI strata despite producing only modest weight loss; notably, a randomized trial in patients without cardiovascular or metabolic comorbidity showed no additional benefit, whereas benefit was observed in patients with type 2 diabetes and heart failure. Third, glucagon-like peptide-1 receptor agonists (GLP-1RA) achieve greater weight loss but yield inconsistent recurrence data, and Mendelian randomization suggests their cardiometabolic benefit is largely BMI-mediated, whereas that of SGLT2i is weight-independent. Together, these observations are consistent with a working hypothesis of two partly distinct atrial substrates—an obesity-related substrate responsive to weight reduction, and a metabolic-inflammatory substrate that may respond to SGLT2i predominantly when metabolic comorbidity is present. This framework is hypothesis-generating: it rests on indirect, cross-study comparisons and has not been tested by formal mediation analysis. If confirmed, it would imply that the two interventions are complementary rather than interchangeable. Full article

Music-to-dance generation requires precisely aligning movement dynamics with musical rhythm, yet existing methods rely on shallow conditioning or auxiliary beat-alignment objectives that fail to establish stable beat–motion correspondences. We present ChoreDiffusion, a diffusion-based framework that integrates explicit beat guidance directly into the denoising process. Central to our approach is a beat-enhanced cross-modal attention mechanism that injects beat-salience cues at every refinement step, promoting fine-grained synchronization beyond the reach of conventional conditioning pipelines. To support multiple dance styles within a unified model, we incorporate lightweight low-rank adaptation (LoRA) modules that encode style-specific motion signatures with only a small set of additional parameters per style, and a three-stage progressive curriculum stabilizes the joint learning of rhythmic alignment and stylistic expressivity. Experiments on two public multi-style dance benchmarks (AIST++ and FineDance) show that ChoreDiffusion achieves the lowest FID values among the compared generation methods on both benchmarks, while maintaining competitive rhythm alignment and multi-style controllability. These results indicate that embedding beat-aware guidance during generation, rather than applying it afterwards, is an effective route toward human-like musicality in music-driven choreography. Full article

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation and joint destruction. Cellular senescence contributes to chronic inflammation, yet key senescence-associated regulators in RA remain unclear. This study aimed to identify RA senescence-related signatures and their roles. Using GSE89408 as the training cohort, we screened hub genes by intersecting differentially expressed and senescence-related genes via WGCNA and three machine learning algorithms, with GSE55457 for external validation. Immune infiltration, regulatory network, subtyping and drug prediction were analyzed. Clinical and in vitro assays validated RIPK2 expression and function in the macrophage senescence-like phenotype, with preliminary signaling exploration. Three senescence-related hub genes (TNFAIP6, SLC2A3, RIPK2) were identified. The derived nomogram showed robust diagnostic performance (AUC = 0.988). Hub genes correlated strongly with myeloid cells, especially macrophages. Two immunologically distinct RA subtypes were identified. RIPK2 was upregulated in clinical samples; its inhibition attenuated LPS-induced macrophage senescence-like changes and inflammation. Preliminary data suggested RIPK2 may act via the NF-κB pathway. This study identifies RA senescence-associated signatures, revealing RIPK2 linking innate immunity to macrophage senescence-like changes, offering novel insights into pathogenesis and supporting it as a candidate biomarker and therapeutic target. Full article

Age-associated mitochondrial decline reduces NAD⁺ availability, impairs oxidative phosphorylation (OXPHOS), and leads to accumulation of reactive oxygen species (ROS) thereby reshaping cellular metabolism. However, the regulatory logic coupling mitochondrial aging to metabolic dysregulation resulting in tumorigenic cell-fate transitions has not been modeled systematically. In this work, we propose a Boolean biomolecular network model of mitochondrial aging and integrate it with metabolic, cell-cycle, and apoptotic biomolecular networks comprising 94 nodes and 370 edges. We then examined how NAD⁺ decline, hypoxia and extracellular ROS shifts the balance between OXPHOS and glycolysis. To this end, the consolidated network model underwent dynamical analysis to elucidate the system-level outcomes as well as its molecular triggers. In particular, we investigated whether the metabolic phenotypes are reversible and how cancer-driver perturbations act in the absence of extracellular pyruvate. The model recapitulates a quiescent, OXPHOS-leaning baseline and predicts that progressive NAD⁺ decline lowers OXPHOS propensity (0.686 to 0.186) while raising glycolysis (0.256 to 0.426). Hypoxia and extracellular ROS synergize glycolytic and hybrid oxidative–glycolytic (W/O) states. Furthermore, these two triggers, together with elevated mitogenic signaling, give rise to a hyperproliferative, glycolytic, and apoptosis-resistant cellular state. Interesting, this state is conditionally reversible wherein receptor tyrosine kinase (RTK) inhibition redirects this cell fate toward apoptosis and collapses the W/O state. Cancer-driver analysis further indicates that, without extracellular pyruvate, VHL loss and RAS, PI3K, or AKT activation preferentially stabilizes glycolytic and hybrid states. Age-resolved TCGA-BRCA analysis provided expression-level support for the predicted remodeling, with declining OXPHOS-associated expression and concurrent OXPHOS/glycolysis activity in older Basal-like tumors. Together, our results show that mitochondrial aging is a priming condition whose tumor-permissive metabolic output is gated by microenvironmental and nutrient inputs. The model provides a novel framework for evaluating age-associated metabolic reprogramming and predicting early tumorigenic cell fates. Full article

Glucagon-like peptide (GLP)-1 receptor agonists (GLP-1RAs) (including medications that contain GLP-1 and other RAs), hereafter referred to as GLP-1 medicines, have significantly advanced the management of metabolic disease and weight management. Obesity is highly prevalent among cancer survivors at the time of diagnosis, and cancer treatments are associated with subsequent changes in weight, either gain or loss. Research has shown that obesity can adversely affect cancer treatment outcomes and survivorship, leading researchers to investigate the potential integration of GLP-1 medicines into oncology care. There is growing interest in understanding the effects of GLP-1 medicines on weight loss and cancer-related outcomes among individuals with obesity who are taking anticancer therapies, as well as individuals treated for cancer in the past who are long-term survivors. This review examines the literature to characterize what is known about GLP-1 medicine use among cancer survivors. The current literature, though limited and largely retrospective, suggests that GLP-1 medicines may contribute to weight loss among cancer survivors, with outcomes varying by cancer stage and type of anticancer therapy. It is important for healthcare providers to consider the potential negative impact of these GLP-1 medications on their patients, especially those with cancer cachexia or sarcopenic obesity, as well as those undergoing anticancer treatments that often lead to weight loss. While there is preclinical evidence suggesting that there are weight-loss independent effects that may be beneficial to individuals with cancer, use of GLP-1 medicines in patients of normal weight for reasons other than treatment of type 2 diabetes should be initiated with caution. On the positive side, these agents may help mitigate therapy-related toxicities, such as cardiotoxicity, with the potential to enhance survivorship outcomes. Unfortunately, there is a notable lack of well-designed randomized controlled trials evaluating the effects of GLP-1 medicines on weight loss, clinical endpoints, and cancer-related outcomes. Advancing the field requires a focus on elucidating the interactions between GLP-1 medicines and anticancer therapies, particularly their impact on treatment efficacy, nutritional status, and overall patient outcomes, both during treatment and in the long term. Full article

Background/Objectives: Obstructive sleep apnea (OSA) is a highly prevalent sleep-related breathing disorder caused by recurrent upper-airway collapse during sleep, leading to intermittent hypoxia, sleep fragmentation, and excessive daytime sleepiness. Although continuous positive airway pressure (CPAP) remains the first-line therapy, long-term adherence is often suboptimal, underscoring the need for more tolerable and flexible treatment options. This review aims to summarize the pathophysiological rationale for pharmacotherapy in OSA and to discuss recent developments in drug-based interventions. Methods: We conducted a narrative review of the literature on pharmacological interventions for OSA, with a systematic search of PubMed, Embase, Cochrane Library, and ClinicalTrials.gov up to 4 August 2026. We included randomised controlled trials, observational studies, meta-analyses, and mechanistic human or animal studies that reported relevant sleep and respiratory outcomes, and graded evidence according to the principles of GRADE framework. Results: Several drug classes have shown promise: agents that increase upper-airway dilator muscle activity, respiratory stabilizers that reduce loop gain, medications that raise the arousal threshold, topical anti-inflammatory drugs for mucosal edema, and systemic metabolic modulators such as glucagon-like peptide-1 receptor agonists and dual incretin receptor agonists. Emerging strategies, including gene therapy directed at the hypoglossal motor system, are also under investigation at the preclinical stage. Moreover, combining pharmacotherapy with CPAP or other devices can produce synergistic benefits, enabling lower device pressures and enhanced patient comfort. Conclusions: Pharmacotherapy for OSA is progressively moving from exploratory research towards targeted, phenotype-driven personalized treatment. Future studies should focus on robust patient phenotyping, multi-mechanistic combination regimens, and long-term clinical outcome evaluations to facilitate the integration of drug-based therapies into routine OSA management, particularly in specific subgroups such as those with COMISA. Full article

Objectives: The role of Phosphoglycerate Dehydrogenase (PHGDH), the first key enzyme in the serine biosynthesis pathway, is important in controlling cancer survival; however, its role in rheumatoid arthritis (RA) remains unknown. Here, we investigated the functional involvement of PHGDH in RA pathogenesis, as well as its underlying molecular mechanisms. Methods: mRNA and protein expression in RA fibroblast-like synoviocytes (FLS) was measured by RT-qPCR and Western blot, respectively. Immunohistochemistry (IHC) was used to detect the protein expression in RA synovium. Cellular and tissue localization of the protein was assessed using IHC and immunofluorescence. The functional role of PHGDH in RA FLS was evaluated using multiple approaches: Transwell assays to assess cell migration and invasion, Annexin V/PI staining to detect apoptosis, and EdU assays to measure cell proliferation. Key downstream targets of PHGDH were identified via RNA sequencing (RNA-seq). The therapeutic potential of PHGDH targeting was further assessed in a rat collagen-induced arthritis (CIA) model following intra-articular administration of PHGDH-shRNA. Results: PHGDH expression was markedly elevated in RA synovial tissues and FLS. Functionally, knockdown of PHGDH suppressed proliferation, migration, invasion, and inflammatory cytokine production of RA FLS. Mechanistic studies revealed that PHGDH exerts its effects, at least in part, by inhibiting the expression of adrenoceptor alpha 2A (ADRA2A). The therapeutic relevance of these findings was further supported by in vivo experiments, where intra-articular delivery of PHGDH-shRNA significantly ameliorated the severity of arthritis in rats with CIA. Conclusions: Our results indicate that the PHGDH-ADRA2A axis critically drives the inflammatory and aggressive phenotype of RA FLS, suggesting that PHGDH might be as a promising therapeutic target for RA. Full article

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) and the dual GIP/GLP-1 co-agonist tirzepatide are increasingly prescribed for obesity and type 2 diabetes in populations enriched for binge-spectrum eating pathology. A recurring controversy asks whether these agents treat eating pathology or merely mask it. This critical narrative review argues that, posed as a simple binary, the question is under-specified, and reframes it around three problems. The central is a measurement problem: several intended effects of GLP-1 RAs are scored as improvement by eating-disorder instruments, creating a diagnostic blind spot. In the one disorder where a weight-acting drug has been tested against a placebo, efficacy on weight coincided with no effect on the psychological core—the dissociation that confounds measurement during GLP-1 RA therapy. The second is a phenotype problem: because BED subtypes already moderate response to drug versus psychological treatment, an agent acting on appetite and reward should not act uniformly, though this remains a hypothesis. The third concerns the post-discontinuation trajectory, and a therapy–harm asymmetry emerges across the spectrum. A factorial, phenotype-stratified trial with disorder-core endpoints and drug-free follow-up could resolve these questions; meanwhile, prudent practice combines uncontaminated pre-treatment screening, monitoring not reliant on confounded self-report, discontinuation planning, and integration with psychological care. Full article

Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are transforming obesity management, yet landmark trials often incompletely measure and report a central mediator of response: dietary intake. Because GLP-1RAs promote weight loss primarily by suppressing appetite and reducing energy consumption, capturing changes in dietary intake is essential to interpreting efficacy, safety, and translation into clinical care. This perspective argues that failure to measure and report comprehensive dietary intake raises concerns under four core bioethical principles. It undermines autonomy by limiting evidence for shared decision-making across the treatment continuum. It challenges non-maleficence because inadequate energy, protein, and micronutrient intake may contribute to lean mass loss and nutrient deficiencies, particularly in vulnerable populations. It weakens beneficence because failing to report a measurable mediator diminishes the scientific value of research requiring substantial investment and participant burden. It raises justice concerns because the equitable distribution of assessment burden and access to resulting nutritional care cannot be evaluated without transparent reporting. To meet the ethical and scientific obligations of clinical research, future trials should preregister dietary intake as a key secondary or safety endpoint. Investigators should report total energy, macronutrient, and micronutrient distribution at baseline and serial follow-up alongside dietary assessment methods, food composition databases, and assessor training. Journal editors, funders, and regulatory bodies should support development of consensus-based, nutrition-specific reporting recommendations aligned with CONSORT principles and encourage preregistration of dietary trial endpoints. Registered dietitian nutritionists should be prospectively integrated into GLP-1RA trial teams from design through data interpretation. Advancing the standard of obesity care requires that the research community look beyond the scale and ground clinical translation in the nutritional context in which pharmacotherapy operates. Full article

Background/Objectives: Juvenile myelomonocytic leukemia (JMML) is a rare, highly aggressive form of pediatric myelodysplastic/myeloproliferative neoplasm characterized by molecular heterogeneity and constitutive activation of the RAS signaling pathway. This study aimed to characterize the mutational landscape, driver genes, mutational signatures, functional pathways, and therapeutic potential of mutated epigenetic regulator genes in JMML. Methods: Tumor and matched buccal swab samples were collected from 35 JMML patients, and whole-exome sequencing was performed. Somatic variants were called with GATK-Mutect2 and annotated with ANNOVAR. maftools and OncodriveCLUST were used for mutational profiling, co-occurrence analysis, driver gene identification, and protein domain mapping. Drug–gene interactions were explored using DGIdb, mutational signatures for genes were characterized by MutationalPatterns, and functional enrichment analysis was performed by the clusterProfiler package. Results: A total of 28 variants were detected in epigenetic regulator genes, with missense mutations being the most common class of variants and a C>T nucleotide substitution pattern being the most frequent. EP300, SETD2, and DNMT3B were the genes most frequently altered, with 8.57% of cases each, followed by ASXL1, BCORL1, ATRX, KMT2A, and TET2 (5.71% each). Driver gene analysis identified ASXL1 as the top candidate driver gene, followed by BCORL1, EP300, and SETD2. Functional enrichment analysis revealed a high number of genes involved in chromatin organization, histone modification, transcriptional regulation, and oncogenic signaling pathways. The mutational signatures identified were SBS5-like, which are dominated by C>T and T>C transitions, indicating endogenous mutational processes. Analysis of drug–gene interactions revealed KMT2A, EP300, and ATRX as the most interconnected and potentially actionable therapeutic targets. Conclusions: This study provides a comprehensive characterization of epigenetic regulator gene alterations in JMML and highlights the importance of epigenetic dysregulation in disease pathogenesis. Full article

RASopathies are a group of genetic disorders caused by germline variants affecting the RAS/MAPK pathway. Their shared phenotypic features—craniofacial anomalies, cardiac defects, cutaneous findings, neurodevelopmental issues, and cancer predisposition—make diagnosis challenging, especially since most lack standardized clinical criteria. This study aimed to develop a practical diagnostic algorithm based on high-frequency Human Phenotype Ontology (HPO) features. Key clinical variables for each RASopathy were identified through HPO, PubMed, and GeneReviews. Only findings present in 80–99% of cases or supported by expert consensus were included. A decision-tree algorithm was constructed and preliminarily evaluated using a blinded cohort of 50 individuals with confirmed molecular diagnoses. Patients were eligible for inclusion if they met the following criteria: (1) molecularly confirmed diagnosis of a RASopathy by next-generation sequencing identifying a pathogenic or likely pathogenic variant; (2) availability of complete phenotypic records in the institutional clinical database; and (3) age at evaluation between 0 and 18 years. Patients were excluded if phenotypic data were incomplete or if molecular confirmation was absent. The algorithm integrates phenotypic patterns and genotype–phenotype correlations. Validation showed 78% accuracy (95% CI: 64.0–88.4%) for clinical diagnosis and 66% accuracy (95% CI: 51.2–78.8%) for molecular prediction. To our knowledge, this is the first HPO-based diagnostic algorithm for the clinical and molecular approach to RASopathies. It provides a structured, accessible tool to improve early recognition and guide molecular testing, particularly for the RASopathy subtypes represented in the validation cohort. Further external validation including underrepresented subtypes is required. Full article

Background/Objectives: Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age, characterised by hyperandrogenism, ovulatory dysfunction, and metabolic disturbances. Semaglutide, a glucagon-like peptide-1 receptor agonist (GLP-1RA), has emerged as a promising therapeutic option for weight management and metabolic optimisation in PCOS. This scoping review evaluates the efficacy and safety of semaglutide in women with PCOS, with pre-specified primary outcomes (weight loss, metabolic parameters) and secondary outcomes (menstrual cyclicity, hormonal regulation, ovarian function, safety). Methods: A systematic literature search was conducted across four electronic databases (SciSpace Deep Search, SciSpace Full Text, Google Scholar, and PubMed) from inception through July 2026. Studies were included if they evaluated semaglutide in women with confirmed PCOS and reported outcomes related to weight loss, hormonal regulation, metabolic parameters, ovarian function, or safety. Two independent reviewers screened 356 unique records; 28 reports were assessed for eligibility, of which full-text access was confirmed for 5, and the remaining 23 were assessed using published abstracts or conference summaries. Two additional records were subsequently excluded due to unverifiable source identification, yielding a final corpus of 25 studies. The review adhered to the PRISMA-ScR reporting guidelines. Results: Twenty-five studies met the inclusion criteria. Semaglutide produced clinically relevant weight reduction (mean 7.6–11.5 kg over 3–6 months; ≥5% weight loss in approximately 80% of patients in responsive cohorts) with concurrent improvements in fasting insulin and HOMA-IR, based predominantly on observational and small-sample study designs. Improvements in menstrual regularity were reported by several studies; however, these data derive largely from conference abstracts or small pilot studies and should be interpreted cautiously. Gastrointestinal adverse events were the most frequent side effects, generally mild-to-moderate and transient. Important safety considerations include gallbladder disease, pancreatitis, and the risk of inadvertent pregnancy exposure following the potential restoration of ovulatory function; semaglutide must be discontinued before planned conception. Conclusions: Based on preliminary evidence from heterogeneous and predominantly low-quality studies, semaglutide shows potentially beneficial effects on weight, metabolic health, and menstrual regularity in women with PCOS. Confirmatory data on ovulation rates, reproductive outcomes, and long-term safety from large-scale RCTs with standardised endpoints are needed before definitive clinical recommendations can be made. Full article

Backgroundand Objectives: Endometrial cancer ranks among the most prevalent gynecologic malignancies in high-income countries, with increasing incidence and mortality driven by the global obesity epidemic. Evidence suggests that women with early-stage disease face a greater risk of death from obesity-related comorbidities than from cancer recurrence and that weight reduction is associated with improvements in quality of life and in the long-term burden of obesity-related morbidity and mortality. Minimally invasive (MIS) metabolic/bariatric surgery is the most effective treatment for achieving significant, sustained weight loss and comorbidities resolution/improvement. Advances in MIS (laparoscopic, robotic, and endoscopic) techniques have reduced perioperative morbidity and mortality. Novel pharmacotherapies, including glucagon-like peptide-1 receptor agonists (GLP-1RAs), have recently received regulatory approval for weight management and ongoing studies are investigating their therapeutic impact on endometrial carcinogenesis and tumor biology. This review synthesizes and critically appraises evidence on metabolic interventions, including innovative bariatric techniques and pharmacologic agents, with the aim of informing their integration into multidisciplinary, risk-adapted management strategies for patients with severe obesity and endometrial cancer. Materials and Methods: A comprehensive review was conducted in accordance with SANRA (Scale for the Assessment of Narrative Review Articles) criteria. Results: Emerging evidence indicates that MIS metabolic/bariatric surgery combined with hysterectomy is feasible and may be integrated into the multidisciplinary management of selected patients with severe obesity and endometrial hyperplasia or carcinoma. GLP-1RAs may modulate both the obesogenic systemic milieu and selected tumor-associated pathways, although definitive clinical evidence of direct antitumor effect and oncologic benefit in endometrial cancer has not been established. Conclusions: Obesity is a modifiable risk factor for endometrial cancer. Metabolic/bariatric interventions represent a promising component of the comprehensive, patient-centered management of this disease. Prospective studies are essential to clarify the association between these interventions and longitudinal oncologic outcomes, the feasibility and potential benefits of combined approaches, and their differential impact according to the molecular classification of endometrial cancers. Although weight reduction is associated with a lower risk of endometrial cancer, a direct improvement in cancer-specific survival has not yet been demonstrated; weight-loss management therefore represents a promising component of care in the severely obese population, and its incorporation into formal guidelines requires confirmation in prospective studies. Full article

Glucagon-like peptide 1 receptor agonists (GLP-1RAs) have revolutionized the management of not only type 2 diabetes but also obesity. However, even with rapid therapeutic advances in GLP-1RAs, questions regarding the fundamental principles of GLP-1-mediated weight loss and the enhanced efficacy of next-generation therapies remain. In this comprehensive review article, we first examine the milestones of GLP-1, from its initial discovery and biological characterization to its successful translation into clinical therapy. Furthermore, this review highlights the latest clinical trial data, specifically HbA1c reduction, weight-loss efficacy, and safety profiles, while exploring current pipelines of major pharmaceutical companies. Additionally, we delineate the mechanistic principles underlying the efficacy of GLP-1 single- and multi-receptor agonists and address challenges in mitigating side effects of GLP-1RAs. Finally, we analyze the rapidly evolving landscape of next-generation, incretin-based combination therapies. With an abundance of GLP-1- related therapies already available or in development, we assess how future GLP-1 multi-receptor agonists can achieve enhanced efficacy and how leveraging weight-loss biology, such as set-point theory, can improve therapeutic outcomes. Full article

Background: Asthma is a chronic inflammatory airway disease characterized by variable airflow obstruction and tissue remodeling. Alamandine (ALA), a renin–angiotensin system (RAS) peptide with anti-inflammatory properties, remains poorly explored in allergic respiratory disease. Objectives: This study evaluated prophylactic (33 days) and therapeutic (21 days) subcutaneous ALA (50 µg/kg/day) administration in an ovalbumin (OVA)-induced rat asthma model. Methods: Twenty male Wistar rats were assigned to four groups: control (CO), OVA with prophylactic ALA (ALA-P; days 1–33), OVA with therapeutic ALA (ALA-T; days 12–33), and OVA-only control (OVA). Rats were sensitized (days 1–3) and challenged with aerosolized OVA (days 6–33). On day 34, ventilatory mechanics were assessed via FlexiVent, including methacholine challenge (12.5 mg/mL). Pulmonary inflammation was evaluated by eosinophil quantification; MrgD/Mas and AT1 receptor expression by immunohistochemistry and Western blot, respectively. Results: OVA animals exhibited elevated baseline airway resistance and bronchoconstriction, and eosinophil infiltration. ALA-T significantly attenuated the respiratory symptoms, restoring airway resistance and eosinophil infiltration to CO-group levels, whereas ALA-P exhibited only a partial reduction. MrgD and Mas expression were elevated in OVA, reflecting compensatory RAS activation, but normalized in both ALA-treated groups. No significant differences in AT1 expression were observed. Conclusions: ALA likely exerts bronchoprotective and anti-allergic effects in this model via MrgD/Mas modulation. The ALA–MrgD/Mas axis represents a potential therapeutic target for allergic airway diseases, particularly when conventional treatments are insufficient. Full article