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Updated: Jul 10, 2026

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
Published on: September 26, 2018
Metalloproteinases and vulnerable atherosclerotic plaques
1University of Bristol, Bristol Heart Institute, Bristol Royal Infirmary, Bristol BS2 8HW. a.newby@bris.ac.uk
Plaque rupture, leading to heart attacks and strokes, involves weakened fibrous caps due to matrix metalloproteinases (MMPs). Therapies must target harmful MMP activity to prevent dangerous plaque rupture.
Area of Science:
- Cardiovascular Biology
- Biochemistry
- Pathology
Background:
- Plaque rupture is a primary cause of myocardial infarctions and strokes.
- Ruptured plaques are characterized by thin, inflamed, and collagen-poor fibrous caps.
- Elevated levels of proteases, such as matrix metalloproteinases (MMPs), are found in weakened plaque caps.
Purpose of the Study:
- To investigate the dual role of matrix metalloproteinases (MMPs) in plaque stability and rupture.
- To explore therapeutic strategies targeting MMPs in cardiovascular disease.
Main Methods:
- Analysis of plaque composition and protease levels.
- Assessment of MMPs' effects on fibrous cap integrity.
- Evaluation of vascular smooth muscle cell migration and proliferation.
Main Results:
- MMPs can weaken fibrous caps by degrading extracellular matrix components.
- MMPs also promote vascular smooth muscle cell migration and proliferation, potentially stabilizing caps.
- The net effect of MMPs on plaque stability is complex and context-dependent.
Conclusions:
- Matrix metalloproteinases (MMPs) play a dual role in atherosclerotic plaque stability, potentially contributing to both rupture and stability.
- Therapeutic interventions should selectively target detrimental MMP activity or its causative factors to prevent plaque rupture.
- Further research is needed to elucidate the precise mechanisms and develop targeted therapies.
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