ReviewCurrent atherosclerosis reports2025
The Role of the PI3K/Akt/mTOR Pathway in Atherosclerosis: Mechanisms, Therapeutic Potential, and Emerging Targeted Treatments.
Review in Current atherosclerosis reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Review
- Research Progress on the Molecular Mechanism of LRP1 and TGFβ-PDGFRβ Signaling Network in Atherosclerosis and Vascular Remodeling.International journal of molecular sciences · 2026Review
- Neointimal hyperplasia and vascular restenosis: from molecular mechanisms to therapeutic interventions.Molecular biomedicine · 2026Review
- α-Hederin Alleviates Endoplasmic Reticulum Stress by Upregulating TRIM38 Expression, Thereby Inhibiting Hepatic Stellate Cell Activation and Liver Fibrosis.Biomedicines · 2026Article
- Pathological mechanisms of inflammatory responses in atherosclerosis and the multi-target regulatory effects of traditional Chinese medicine.Frontiers in cardiovascular medicine · 2026Review
- Mechanisms of Yiqi Huoxue Granule in Atherosclerosis Treatment: Insights from UPLC-Q-Exactive Orbitrap-MS Analysis, Network Pharmacology, Molecular Docking, and Experimental Verification.Journal of inflammation research · 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
4 authors.
Funding
Abstract
purpose of reviewThe PI3K/Akt/mTOR (phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin) signaling pathway is pivotal in regulating cellular functions such as growth, proliferation, survival, and metabolism. Dysregulation of this pathway contributes to the pathogenesis of multiple diseases, including cancer, metabolic disorders, and cardiovascular diseases, notably atherosclerosis. This review outlines the role of the PI3K/Akt/mTOR pathway in the progression of atherosclerosis, emphasizing its involvement in endothelial protection, vascular smooth muscle cell proliferation and migration, as well as inflammatory modulation. RECENT
findingsThe pathway affects atherosclerosis through several mechanisms: it both protects and can harm the blood vessel lining, controls how muscle cells in vessel walls grow, move and die, and influences inflammation. These processes critically affect how plaques form, become unstable, and progress. Current drug treatments and procedures targeting this pathway show promise, though existing therapies often lack specificity. Understanding the many roles the PI3K/Akt/mTOR pathway plays in atherosclerosis offers important insights for creating targeted treatments. While current approaches show potential, we urgently need new interventions that specifically target this pathway to address heart disease complexity and improve patient results. Future studies should focus on developing more precise treatments to effectively reduce atherosclerosis.
Indexed as
Identifiers
41240276What 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.