ReviewMolecular biology reports2025
Insights on inflammatory pathways and their cross-talk: a comprehensive review on asthma.
Review in Molecular biology reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Review
- The lung microbiome and asthma: from inflammatory phenotype differentiation to microbe-based immunomodulatory strategies.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Allergic asthma is a heterogeneous respiratory disease characterized by recurring chest tightness, wheezing, coughing, and shortness of breath. Inflammation in asthma can be characterized into two types: T2 inflammation (Eosinophilic asthma) and non-T2 inflammation (Neutrophilic asthma). T2 inflammation is mediated by T helper type 2 cells (Th2) And innate lymphoid type 2 cells (ILC2), whereas the involvement of neutrophils, macrophages, and cytokines such as IL-2, IL-6, and IL-17 characterizes non-T2 inflammation. Asthma pathophysiology is complexly linked to the dysregulation of key intracellular signaling pathways, including NF-κB, JAK-STAT, MAPK, PI3K, and Nrf2. NF-κB plays an important role in the maintenance of the chronic inflammatory response by increased expression of cytokines in the airway epithelium. In contrast, the MAPK signaling pathway, through the involvement of MAPKs, which belong to the family of serine/threonine protein kinases, contributes to inflammatory responses through responding to various stimuli such as osmotic stress, heat shock, mitogens, and the inflammatory cytokines, which result in the regulation of cell proliferation, cell survival, cell differentiation, and apoptosis. JAK-STAT signaling mediates cytokine responses critical for Th2-driven asthma phenotypes, while the PI3K pathway exacerbates inflammation and oxidative stress through several processes, e.g., cell growth, proliferation, survival, differentiation, and migration. Conversely, the Nrf2 pathway is a protective mechanism, regulating antioxidant defenses to counter oxidative damage in asthmatic airways. Exploring the interesting crosstalk between these pathways offers profound insights into asthma's intricate molecular mechanisms, thereby paving the way for targeted and personalized therapeutic interventions.
Indexed as
Identifiers
41174322What OpenQuestion 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 OpenQuestion graph.