ArticleBlood2018
AMPK-ACC signaling modulates platelet phospholipids and potentiates thrombus formation.
Article in Blood, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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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.
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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.
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Who cites it
48 citing papers in PubMed, 85 citations in OpenAlex.
- Platelet characteristics in extremely preterm infants after fatty acid supplementation: a randomized controlled trial.Pediatric research · 2025Trial
- De novo lipogenesis is essential for platelet production in humans.Nature metabolism · 2020Trial
- miR-146a mimic therapy protects against platelet-mediated thrombosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- 1,1-Diethoxyethane enhances aerobic respiration in human mitochondria via activation of AMP-activated protein kinase.Communications biology · 2026Article
- Platelet lipidome alterations in septic shock: a matched case-control study.Research and practice in thrombosis and haemostasis · 2026Article
- Synergistic Promotion of Triple-Negative Breast Cancer Tumorigenesis and Metastasis by Oral Polystyrene Nanoplastics Exposure via Alloprevotella-Derived Glutamate and Platelet Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Deleting ACC1 in platelets alters phospholipidome and reduces platelet activation and thrombosis in mice.Blood advances · 2025Article
- Emerging Targets, Novel Directions, and Innovative Approaches in Thrombosis Therapy.Aging and disease · 2025Review
- Review
- Vitisin A Outperforms Cyanidin-3-O-Glucoside in Triglyceride Reduction by Modulating Hepatic Lipogenesis and Fatty Acid β-Oxidation.International journal of molecular sciences · 2025Article
- The Lipid-Oxidative Stress Axis: Novel Therapeutic Targets for Podocytopathy.Journal of inflammation research · 2025Review
- Functional interaction between immune checkpoints and lipid metabolism in the development of arteriosclerosis obliterans.Frontiers in immunology · 2025Review
- Platelet lipidomics and de novo lipogenesis: impact on health and disease.Current opinion in hematology · 2024Review
- Fine-tuning AMPK in physiology and disease using point-mutant mouse models.Disease models & mechanisms · 2024Review
- Immunometabolism in atherosclerotic disorders.Nature cardiovascular research · 2024Review
- Metabolic targeting of platelets to combat thrombosis: dawn of a new paradigm?Cardiovascular research · 2023Review
- The mechanism of oleic acid inhibiting platelet activation stimulated by collagen.Cell communication and signaling : CCS · 2023Article
- The impact of lipid metabolism on breast cancer: a review about its role in tumorigenesis and immune escape.Cell communication and signaling : CCS · 2023Review
- The Effect of Extracellular Vesicles on Thrombosis.Journal of cardiovascular translational research · 2023Review
- New insights into activation and function of the AMPK.Nature reviews. Molecular cell biology · 2023Review
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Authors and funding
20 authors at 9 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AMP-activated protein kinase (AMPK) α1 is activated in platelets on thrombin or collagen stimulation, and as a consequence, phosphorylates and inhibits acetyl-CoA carboxylase (ACC). Because ACC is crucial for the synthesis of fatty acids, which are essential for platelet activation, we hypothesized that this enzyme plays a central regulatory role in platelet function. To investigate this, we used a double knock-in (DKI) mouse model in which the AMPK phosphorylation sites Ser79 on ACC1 and Ser212 on ACC2 were mutated to prevent AMPK signaling to ACC. Suppression of ACC phosphorylation promoted injury-induced arterial thrombosis in vivo and enhanced thrombus growth ex vivo on collagen-coated surfaces under flow. After collagen stimulation, loss of AMPK-ACC signaling was associated with amplified thromboxane generation and dense granule secretion. ACC DKI platelets had increased arachidonic acid-containing phosphatidylethanolamine plasmalogen lipids. In conclusion, AMPK-ACC signaling is coupled to the control of thrombosis by specifically modulating thromboxane and granule release in response to collagen. It appears to achieve this by increasing platelet phospholipid content required for the generation of arachidonic acid, a key mediator of platelet activation.
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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.