Atheroma development in the rabbit aorta.
The Response to Injury Theory
Pathogenesis of
Atherosclerosis
Atherosclerosis is a disease process which is triggered by
sometimes subtle physical or chemical insults to the endothelial cell layer of
arteries. The "Response to Injury Theory" now has widespread
acceptance among scientific and medical scholars. This theory holds that the
earliest event in atherogenesistext annotation indicator is injury to the
endotheliumtext annotation indicator, which can be triggered by any number of
insults, either alone or in combination. These include:
- Physical injury or stress as a result of direct trauma or hypertensiontext annotation indicator
- Turbulent blood flow, for example, where arteries branc
- Circulation of reactive oxygen species (free radicals), e.g., from smoking or air pollutants
- Hyperlipidemia (high blood concentrations of LDL or VLDL)
- Chronically elevated blood glucose levels
- Homocysteinemia, which results from an inherited metabolic defect that leads to very high levels of the homocysteine, a metabolite of methionine; high concentrations are toxic to the endothelium.
The Fatty Streak
Fatty streaks are the first signs of atherosclerosis that
are visible without magnification. A fatty streak consists of lipid-containing
foam cells in the arterial wall just beneath the endothelium. It appears as a
yellow discoloration in the artery's inner surface and occurs in the aorta and
coronary arteries of most people by age 20. Over time, these fatty streaks can
evolve into atherosclerotic plaques or they can remain stable or even regress.
The image below on the left is a photograph of the inside of an artery; one can
see a fatty streak beneath the thin endothelial lining of the artery. The
cartoon on the right summarizes the steps by which the fatty streak evolves.
The cartoon on the right also emphasizes the role of
T-lymphocytes, which are also in the intima. They secrete cytokines that induce
smooth muscle cells to migrate from the media to the intima. These smooth
muscle cells also begin to proliferate under the influence of growth factors.
Over time there is a progressive accumulation of lipid and smooth muscle cells,
and eventually the growing lesion begins to raise the endothelium and encroach
on the lumen of the artery. This is depicted in the image below, which shows a
cross-section of an artery the site of an atherosclerotic plaque.
The Growing Atheroma
Stable & Unstable
Plaques
The image below illustrates the evolution of atherosclerotic
plaques and also indicates that there are two possible forms of evolution.
Slowly growing plaques expand gradually due to accumulation of lipid in foam
cells and migration and proliferation of smooth muscle cells. These plaques
tend to stabilize and are not prone to rupture. The so-called fibrin cap on the
lesion matures. In contrast, other plaques grow more rapidly as a result of
more rapid lipid deposition. These have thin fibrin caps that are prone to
rupture. Once a plaque ruptures, it can
trigger an acute thrombosis (clot) by activating platelets and the clotting cascade.
REFERENCE
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(The Injury Theory) additional views by nimmaterial
I have worked with a variety of polymers, specifically the
crystal cholesterol. Except for some examples of polymers; It hardens
and becomes brittle acids. Some members excluding polymers; polymers, hardens
and becomes brittle with the acid effect and softened by the base effect.
Cholesterol is a big molecule, C27H46O. However, it is a single molecule, and thus a
monomer. In cells cholesterol is normally embedded in cell membrane and makes
hydrogen bonds with surrounding molecules.
Cholesterol and cholesterol esters are large molecules. The pH
was not research in the atheromatous plaques. Atheromatous plaques containing
the acid or alkaline content. How to edit this content or regulatory mechanisms are not known.
Plaque acidity may be an additional factor affecting the
stability of atherosclerotic plaque.
Yavuz Yılmaz
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