Related Experiment Video
Updated: May 6, 2026
07:51
Implantation of a Carotid Cuff for Triggering Shear-stress Induced Atherosclerosis in Mice
Published on: January 13, 2012
20.0K
Collagenases and cracks in the plaque.
1Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. plibby@partners.org
The Journal of Clinical Investigation
|August 3, 2013
Summary
Atheromatous plaque rupture, a cause of heart attacks, is linked to collagen-degrading enzymes. These matrix metalloproteinases (MMPs) may destabilize plaque fibrous caps, increasing rupture risk.
Area of Science:
- Cardiovascular biology
- Biochemistry
- Pathology
Background:
- Atheromatous plaques contain lipids and cellular debris, covered by a fibrous cap.
- Plaque rupture is a primary cause of myocardial infarctions.
- Interstitial collagen provides tensile strength to the fibrous cap.
Purpose of the Study:
- To investigate the role of collagenolytic enzymes in atheromatous plaque destabilization.
- To implicate matrix metalloproteinases (MMPs) in plaque rupture.
Main Methods:
- Demonstration of enzyme overexpression in atheromatous plaques.
- Analysis of MMPs' role in lesion destabilization.
Main Results:
- Overexpression of collagenolytic enzymes was observed in atheromatous plaques.
- Matrix metalloproteinases (MMPs) were implicated in the destabilization of these lesions.
Conclusions:
- Collagenolytic enzymes, specifically MMPs, are likely involved in destabilizing atheromatous plaques.
- Targeting MMPs could be a therapeutic strategy to prevent plaque rupture and myocardial infarctions.
Related Concept Videos
01:23Role of Matrix Metalloproteases in Degradation of ECM
2.9K
Matrix metalloproteases (MMPs) are enzymes involved in the hydrolysis of proteins and glycoproteins of the extracellular matrix. MMPs are essential for the migration and proliferation of cells through the dense matrix network, throughout embryonic development, and throughout morphogenesis. The first MMP activity discovered was a collagenase in a tadpole's tail undergoing metamorphosis. The active collagen deposition and modifications lead to the morphogenesis of tadpoles into the adult...
2.9K
01:22Formation of the Platelet Plug
6.3K
The platelet phase, the second stage of hemostasis, commences around 15-20 seconds after an injury. It follows and overlaps with the vascular phase, during which blood vessels constrict to minimize blood loss.
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
As the injured blood vessel contracts, endothelial cells undergo contraction, revealing collagen fibers in the basement membrane and underlying connective tissue. Furthermore, the plasma membrane of endothelial cells becomes adhesive, preparing the site for platelet adhesion. Platelets...
6.3K
01:16Clot Retraction and Fibrinolysis
6.1K
After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
6.1K
01:26Coronary Artery Disease II: Pathophysiology
1.1K
Coronary Artery Disease (CAD) originates from a series of events that impair the function of coronary arteries, the blood vessels responsible for delivering oxygen-rich blood to the heart muscle. The pathophysiology of CAD is closely linked to atherosclerosis, a chronic inflammatory and lipid-driven condition affecting the vascular endothelium.1. Endothelial DamageThe process begins with damage to the vascular endothelium, which serves as a protective barrier between the blood and the vessel...
1.1K
01:30Atherosclerosis I: Introduction
2.5K
Atherosclerosis is a progressive disorder characterized by the buildup of plaques on the arterial inner wall, causing them to narrow and harden over time. These plaques comprise lipids, calcium, blood components, carbohydrates, and fibrous tissue. The process primarily affects the intima of large and medium-sized arteries, reducing blood flow in any artery.Etiology and risk factorsThe cause of atherosclerosis is multifactorial, involving a complex interplay among endothelial injury, lipid...
2.5K
01:23Alzheimer Disease ll: Pathophysiology
44
Alzheimer disease involves structural changes in the brain that begin long before symptoms appear. The most distinctive features are extracellular neuritic plaques and intracellular neurofibrillary tangles.Neuritic plaques form in the cerebral cortex and around blood vessels. These plaques contain a dense core of beta-amyloid (Aβ)—a toxic protein fragment that clumps outside neurons. The core is surrounded by damaged neuronal extensions, as well as reactive astrocytes and...
44