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Hypercoagulability Impairs Plaque Stability in Diabetes-Induced Atherosclerosis
Saira Ambreen1, Sameen Fatima1,2, Ahmed Elwakiel1
1Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostic, University Hospital Leipzig, 04103 Leipzig, Germany.
Nutrients
|May 28, 2022
Summary
Impaired thrombomodulin (TM) function in diabetes reduces atherosclerotic plaque stability. This dysfunction contributes to unstable plaques, increasing mortality risk in diabetic patients.
Area of Science:
- Cardiovascular Biology
- Metabolic Disease Research
- Thrombosis and Hemostasis
Background:
- Diabetes mellitus accelerates atherosclerosis, a leading cause of mortality in diabetic individuals.
- Diabetes-associated atherosclerosis involves reduced endothelial thrombomodulin (TM) expression and impaired activated protein C (aPC) generation.
- Current therapeutic strategies for diabetes-associated atherosclerosis remain insufficient.
Purpose of the Study:
- To investigate the role of impaired thrombomodulin (TM) function in the stability of atherosclerotic plaques in a diabetic mouse model.
- To elucidate the impact of dysfunctional TM on plaque composition and characteristics under hyperglycemic conditions.
Main Methods:
- Utilized hyperglycemic mice expressing dysfunctional TM (TMPro/Pro) crossed with ApoE-/- mice to model diabetes-associated atherosclerosis.
- Analyzed atherosclerotic lesion size, lipid accumulation, necrotic core area, fibrous cap thickness, and immune cell infiltration (macrophages, smooth muscle cells) in the truncus brachiocephalic.
Main Results:
- Diabetic TMPro/Pro ApoE-/- mice exhibited reduced plaque stability compared to diabetic ApoE-/- mice.
- While overall plaque and lumen size were smaller, TMPro/Pro mice showed larger necrotic cores and thinner fibrous caps, indicative of instability.
- Lesions in diabetic TMPro/Pro mice contained more macrophages and fewer smooth muscle cells.
Conclusions:
- Impaired thrombomodulin (TM) function exacerbates atherosclerotic plaque instability in the context of hyperglycemia.
- Dysfunctional TM contributes to a pro-coagulant phenotype and promotes the development of unstable atherosclerotic lesions.
- Targeting TM function may offer a therapeutic avenue for managing diabetes-associated atherosclerosis.
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