ArticleIranian journal of biotechnology2025
Unlocking TB-COPD Pathogenesis: A Biotechnological Approach Targeting the PI3K/Akt Pathway.
Article in Iranian journal of biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: tuberculosis (tb)-health problems caused by chronic obstructive pulmonary disease (copd), as one of the important problems facing global public health, highlight its far-reaching effects. The pi3k/akt signaling pathway is implicated in inflammatory responses and cellular survival, suggesting its potential role in tb-copd pathogenesis. Objective: This study integrated computational and experimental biotechnology approaches to identify key molecular mechanisms linking tb and copd, with a focus on the pi3k/akt signaling pathway. Materials and Methods: By analyzing two publicly available gene expression datasets (gse42057, gse83456), weighted network gene coexpression analysis technology was applied to identify differently expressed genes and key coexpression modules to explore their potential biological relevance and functional associations in more depth. Functional enrichment analysis (go/kegg) was performed to assess pathway involvement. Experimentally, a mycobacterium tuberculosis-infected bronchial epithelial cell model (16hbe) was established, and the pi3k/akt inhibitor ly294002 was utilized to evaluate its effects on apoptosis, proliferation, and epithelial-mesenchymal transition (emt) markers. Results: Weighted correlation network analysis (Wgcna) identified a key module significantly enriched in pi3k/akt signaling. Experimental validation demonstrated that ly294002 treatment significantly improved cell survival (p < 0.05), reduced apoptosis, and restored epithelial integrity. It was found that an increase in epithelial cadherin expression levels was accompanied by a decrease in neuronal cadherin expression levels. This dynamic change shows that the characteristics and patterns of cell adhesion can significantly adapt to certain physiological or pathological processes. Furthermore, ly294002 suppressed pi3k/akt mrna expression and phosphorylation (p < 0.05), confirming pathway inhibition. Conclusion: This study provides a novel biotechnological perspective on the role of pi3k/akt signaling in tb-COPD, highlighting its potential as a therapeutic target. The integrative use of bioinformatics and experimental validation strengthens our understanding of molecular pathogenesis，opens the way to precision medicine strategies in the treatment of respiratory diseases.
Indexed as
Identifiers
What 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.