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Updated: Jul 11, 2025
11:42
Live-cell Imaging of Platelet Degranulation and Secretion Under Flow
Published on: July 10, 2017
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Platelet biology and function: plaque erosion vs. rupture.
Constance C F M J Baaten1,2, Magdolna Nagy1, Wolfgang Bergmeier3,4
1Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, Universiteitssingel 50, 6229 ER, Maastricht, the Netherlands.
European Heart Journal
|November 8, 2023
Summary
Coronary atherosclerosis, a chronic inflammatory process, causes heart disease. Platelets play a key role in thrombus formation and plaque healing, necessitating new antithrombotic agents.
Area of Science:
- Cardiovascular Medicine
- Inflammation Biology
- Hematology
Background:
- Coronary atherosclerosis is a leading cause of heart disease, driven by chronic inflammation, not just aging.
- Atherosclerotic plaque phenotype (rupture vs. erosion) dictates lesion characteristics and clinical event risk.
- Platelet activation and thrombus formation differ based on plaque phenotype.
Approach:
- This review examines plaque phenotype in relation to thrombus composition.
- It overviews mediators of plaque-induced platelet activation: hemodynamics, matrix components, and soluble factors.
- The review summarizes recent findings on plaque healing and platelet involvement.
Key Points:
- Plaque rupture and erosion initiate platelet activation differently.
- Mediators like hemodynamics, matrix components, and soluble factors influence platelet activation.
- Platelets may play a role in plaque healing after disruption.
Conclusions:
- Understanding plaque phenotype is crucial for predicting clinical events.
- Platelet function in thrombus formation and plaque healing requires further investigation.
- There is a clinical need for improved antithrombotic therapies.
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