Atherosclerosis formation
Atherosclerosis literally means hardening of the arteries. This is due to the formation of a atherosclerotic plaque in the wall of the arteries.
Because of this the radius of the lumen of the artery becomes narrow and the blood supply will be hindered, reducing the blood supply to a particular tissue. Thus, leading to the death of the tissue and the malfunction of that particular organ of the body.
If the coronary arteries are affected, the heart will get poor blood supply and will cause a heart attack and if this occurs in a artery blood vessel supplying the brain a stoke will be resulted 😦
Let us now look at how these plaques are being formed…
Before that, a brief idea about the wall of an artery will be useful 🙂
The wall of an artery is formed by 3 layers. From inward -> outward way,
tunica intima- inner most layer containing epithelial cells
tunica media- the middle layer containing smooth muscles
tunica adventitia- the outer most layer mainly containing collagen fibers
Having said that, lets see the process of this…
1) In a person with high LDL (low density lipoproteins) level, LDL can get oxidized.
(because in arteries there is adequate amount of oxygen. Because of this, Oxygen free radicals can also be present in the blood. These free radicals attack LDL and produce Oxidized LDL)
2) Oxidized LDL go inside the tunica intima, that is they go and lodge underneath the epithelial cells covering the lumen of the arterial wall.
3) This oxidized LDL’s apolipoprotein apo-100 binds to the scavenger receptors.
4) This activates the conversion of monocytes into macrophages.
5) These macrophages also go inside the tunica intima (to the place where oxidized LDL is staying)
6)This results in the formation of a “FOAM CELL” (foam cell is simply, macrohages and oxidized LDL)
7) This appears as a fatty streak :}
8) If this process goes on and on for a long time, a scar tissue will be formed.
9) This ongoing process also stimulates cytokines. Cytokines convert the inactive Growth factors (GF) in to active growth factors.
10) And these active GFs result in the proliferation of the smooth muscles in the tunica media layer of the artery wall.
11) Some of the proliferated sooth mucles, also migrate in to the tunica intima. And they will form a fibrous capsule around the plaque.
12) This plaque is highly vulnerable to damage. (in later stages, this plaque can even be calcified with Ca2+ and reduce the flexibility of the blood vessel)
13) If this plaque gets damaged, and ruptured and if collagen is exposed, platelets come and adhere in to it. This will result in the formation of a thrombus.
therefore, the lumen will be narrowed, and the blood supply to the tissue will be obstructed and will ultimately lead to the death of that particular organ in the body…
additional facts-
* Endothelial cells of the blood vessels maintain the vasomotor tone of the blood vessels. hat is they help in vasoconstricion as well as vasodialation. Endothelin produced by the endothelial cells help in maintaining the vasoconstriction and prostacyclin, hyperpolarizing factors and NO (Nitrogen Oxide) help in maintaining the vasodialation.
* Oxgen free radicals eg- superoxides react with NO and produce, Peroxynitrite. Thus, the vasoprotective function of the blood vessels will be lost.
* Activated macrophages also produce- myeloperoxidase, lipooxygenases and NADPH oxidase
So yeah, that’s all the information I have. Please share what you think 🙂
Thank You! =D
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