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Updated: Jun 3, 2026

Ferric Chloride-induced Murine Thrombosis Models
Published on: September 5, 2016
LXR as a novel antithrombotic target
Michael Spyridon1, Leonardo A Moraes, Chris I Jones
1Institute for Cardiovascular and Metabolic Research, University of Reading, Reading, UK.
Liver X receptors (LXRs) regulate cholesterol and have athero-protective effects. LXR ligands non-genomically inhibit platelet aggregation and reduce thrombosis, suggesting LXRs as a target for athero-thrombotic disease prevention.
Area of Science:
- Biochemistry
- Molecular Biology
- Cardiovascular Research
Background:
- Liver X receptors (LXRs) are key regulators of cholesterol homeostasis.
- LXR ligands exhibit athero-protective properties beyond cholesterol metabolism.
- Platelets, crucial in atherosclerosis initiation, express nuclear receptors despite lacking nuclei.
Purpose of the Study:
- To investigate the role of Liver X receptors (LXRs) in human platelets.
- To determine if LXR ligands mediate athero-protective effects through platelets.
- To explore the mechanism of LXR action in platelet function.
Main Methods:
- Detection of LXR-β expression in human platelets.
- Assessment of LXR ligand (GW3965, T0901317) effects on platelet aggregation.
- Analysis of LXR association with signaling molecules (GPVI) in platelets.
- In vivo thrombosis model in mice to evaluate antithrombotic effects of GW3965.
Main Results:
- LXR-β is expressed in human platelets.
- LXR ligands GW3965 and T0901317 non-genomically modulated platelet aggregation.
- GW3965 promoted LXR association with GPVI signaling components.
- GW3965 demonstrated antithrombotic effects in a mouse model, reducing thrombus size and stability.
Conclusions:
- LXR-β plays a role in platelet function.
- LXR ligands exert antiplatelet and antithrombotic effects.
- LXRs represent a potential therapeutic target for preventing athero-thrombotic diseases.
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