SynthesisFrontiers in immunology2026
A molecular systems architecture of asthma.
Synthesis in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed, 1 synthesis or guideline pooled it.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Asthma is a heterogeneous inflammatory disease driven by complex genetic, immunological, environmental, and neuro-immune interactions. Modern therapeutic strategies increasingly target distinct molecular mechanisms underlying specific asthma endotypes. Emerging evidence highlights the role of psychological stress in modulating the neuro-immune axis, contributing to allergic airway inflammation. Systems biology offers a powerful framework to understand the multi-cellular and cross-organ interactions between lung and brain microenvironments that drive asthma pathogenesis. Objective: To develop a molecular systems architecture of asthma using the CytoSolve Methods: A systematic bioinformatics literature review was conducted using Medical Subject Headings (MeSH) across PubMed, Medline, and Google Scholar, covering peer-reviewed publications from January 2008 to August 2025. Relevant full-length articles were curated and analyzed using the CytoSolve Result: The systems architecture identified biomolecular interactions across thirty-one cell types spanning bronchial, immune, stromal, vascular, endocrine, and neuronal compartments, including airway epithelial cells, T-cells, eosinophils, mast cells, fibroblasts, microglia, hypothalamic and brainstem neurons, vagal sensory neurons, and autonomic airway neurons. Environmental triggers such as pollutants and infections initiate cascades that promote three core pathobiological processes: airway inflammation, hyperresponsiveness, and remodeling. Psychological comorbidities, including anxiety and depression, further amplify airway inflammation through brain-lung cross-talk, contributing to neuronal inflammation and asthma exacerbations. Conclusions: This system architecture generated a multilayered visual map that shows the associations between various triggers and biomolecular interactions across airway and neuronal cell types in the lung and brain microenvironment, respectively. The architecture may be utilized for target identification, discovery of single and combination therapeutics, biomarkers, and clinical strategies to treat asthma endotypes.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.