ArticleMolecular and cellular biochemistry2026
Bioelectric fields drive pulmonary epithelial proliferation through PI3K/AKT/GSK3β signaling.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
- Tideglusib-Preactivated Osteoblasts Encapsulated in Ceramic Particle-Reinforced GelMA Hydrogel for Enhanced Critical-Size Bone Defect Regeneration.Drug design, development and therapy · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Defective alveolar re-epithelialization following acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) represents a critical barrier to clinical recovery. Intrinsic signals that could be harnessed to speed this repair remain poorly defined. Endogenous electric fields (EFs) arise immediately after epithelial injury and are recognized as mediators of cell migration and morphogenesis, but their impact on lung epithelial proliferation is unknown. Here we demonstrate that physiological-strength direct-current EFs (100–200 mV/mm) are potent pro-mitogenic signals for both human bronchial (BEAS-2B) and murine alveolar (MLE-12) epithelial cells. Within a custom live-cell electrotactic chamber, EFs exposure for 4 h doubled EdU incorporation, increased Ki-67 expression, and elevated real-time mitotic events without altering spindle orientation. RNA-seq analysis of BEAS-2B cells with EFs exposure identified 1,447 differentially expressed genes, with significant enrichment of the PI3K/AKT signaling pathway and immunoblotting further confirmed rapid phosphorylation of PI3K p85 (Tyr458)/p55 (Tyr199) and AKT (Ser473). Selective inhibition with Alpelisib or LY294002 abolished pathway activation and fully suppressed the pro-proliferative effect of EFs. Furthermore, EFs triggered AKT-dependent phosphorylation of glycogen synthase kinase-3β (GSK3β) at Ser9, while blockade with the GSK3β inhibitor Tideglusib or upstream PI3K inhibitors suppressed this event and attenuated EF-induced proliferation. Taken together, our findings delineate the PI3K/AKT/GSK3β signaling axis through which EFs enhance pulmonary epithelial proliferation. This work identifies physiological EFs as previously unrecognized regenerative cues in the lung and underscores bioelectric modulation as a promising therapeutic strategy to accelerate alveolar repair in ALI/ARDS.
Indexed as
Identifiers
41609898What 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.