ArticleExpert review of hematology2010
Akt signaling in platelets and thrombosis.
Article in Expert review of hematology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 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
69 citing papers in PubMed, 135 citations in OpenAlex.
- Trial
- Ginsenoside Rg1 attenuates platelet activation under shear stress via multi-target suppression of PI3K/AKT and ERK1/2 pathways: an in vitro microfluidic study.Journal of thrombosis and thrombolysis · 2026Article
- Review
- KLF4 Protects Against Sepsis-Induced Coagulopathy via Inhibition of the AKT/mTOR/STAT3 Signaling Pathway.Journal of inflammation research · 2026Article
- Endoplasmic Reticulum Stress-Induced triggering Receptor Expressed on Myeloid Cells 2 (TREM2) Downregulation Exacerbates Platelet Activation and Myocardial Infarction in Patients With Coronary Artery Disease.Journal of the American Heart Association · 2025Article
- Platelet Responses to Urethane Dimethacrylate-Based Bone Cements Containing Monocalcium Phosphate/ε-Polylysine: Role of ε-Polylysine inACS materials Au · 2025Article
- Network pharmacology analysis and clinical verification ofBiomedical reports · 2025Article
- Clinical Potential of Misshapen/NIKs-Related Kinase (MINK) 1-A Many-Sided Element of Cell Physiology and Pathology.Current issues in molecular biology · 2024Review
- Human Disabled-2 regulates thromboxane ANature communications · 2024Article
- O-GlcNAcylation: Crosstalk between Hemostasis, Inflammation, and Cancer.International journal of molecular sciences · 2024Review
- Growing concerns about using hypoxia-inducible factor prolyl hydroxylase inhibitors for the treatment of renal anemia.Clinical kidney journal · 2024Review
- Eugenol Suppresses Platelet Activation and Mitigates Pulmonary Thromboembolism in Humans and Murine Models.International journal of molecular sciences · 2024Article
- Inverse relationship between platelet Akt activity and hippocampal atrophy: A pilot case-control study in patients with diabetes mellitus.World journal of clinical cases · 2024Article
- Evidence that inositol 1,4,5-trisphosphate 3-kinase and inositol 1,3,4,5-tetrakisphosphate are negative regulators of platelet function.Research and practice in thrombosis and haemostasis · 2024Article
- The emerging Janus face of SVEP1 in development and disease.Trends in molecular medicine · 2023Review
- The mechanism of oleic acid inhibiting platelet activation stimulated by collagen.Cell communication and signaling : CCS · 2023Article
- Article
- SVEP1 is an endogenous ligand for the orphan receptor PEAR1.Nature communications · 2023Article
- The Intricate Role of Non-Coding RNAs in Sepsis-Associated Disseminated Intravascular Coagulation.International journal of molecular sciences · 2023Review
- Dematin Regulates Calcium Mobilization, Thrombosis, and Early Akt Activation in Platelets.Molecular and cellular biology · 2023Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Akt is a Ser-Thr kinase with pleiotropic effects on cell survival, growth and metabolism. Recent evidence from gene-deletion studies in mice, and analysis of human platelets treated with Akt inhibitors, suggest that Akt regulates platelet activation, with potential consequences for thrombosis. Akt activation is regulated by the level of phosphoinositide 3-phosphates, and proteins that regulate concentrations of this lipid also regulate Akt activation and platelet function. Although the effectors through which Akt contributes to platelet activation are not definitively known, several candidates are discussed, including endothelial nitric oxide synthase, glycogen synthase kinase 3β, phosphodiesterase 3A and the integrin β(3) tail. Selective inhibitors of Akt isoforms or of proteins that contribute to its activation, such as individual PI3K isoforms, may make attractive targets for antithrombotic therapy. This review summarizes the current literature describing Akt activity and its regulation in platelets, including speculation regarding the future of Akt or its regulatory pathways as targets for the development of antithrombotic therapies.
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.