ReviewJournal of molecular histology2026
The impact of the PI3K/AKT pathway on arrhythmia: mechanisms of action and therapeutic potential.
Review in Journal of molecular histology, 2026. 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.
- A large-scale single-nucleus resource reveals a cardiomyocyte-like fibroblast and stage-specific remodeling across cardiomyopathies.BMC medicine · 2026Article
- Mechanisms and therapeutic potential of glycyrrhizic acid: Insights into key signaling pathways and disease modulation (Review).Molecular medicine reports · 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
6 authors.
Funding
Abstract
Arrhythmias, driven by abnormal electrical activity and structural remodeling, are a leading cause of cardiovascular mortality. Despite advances in treatment methods, therapeutic limitations persist due to an incomplete understanding of the heterogeneous mechanisms involved. The phosphoinositide 3-kinase/protein kinase B (PI3K/AKT) signaling pathway, a central regulator of cellular survival, metabolism, and electrophysiology, has been identified as a key factor in arrhythmia development. This review summarises evidence indicating that dysregulated PI3K/AKT signaling promotes arrhythmias via four interconnected pathways: electrophysiological remodeling, oxidative stress and inflammation, autophagy and apoptosis, and fibrotic structural remodeling. Notably, under certain conditions, the PI3K/AKT signaling pathway exhibits bidirectional regulatory effects. Furthermore, evidence suggests that pharmacologically targeting the PI3K/AKT pathway exhibits significant anti-arrhythmic potential.
Indexed as
Identifiers
41572093What 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.