The LDL molecules can pass in and out of the intima? What are relative sizes of the LDL and the spaces you are referring to? Certainly they are not entering the cell walls of the intimal cells.
Hello. Not directly, not by itself. They are transported throught the endocytosis. In a normal situation there are special receptors for LDL in the cells which make cholesterol transport into the cell possible. When the acummulation of LDL is so high that your receptors are too slow to absorb all of them ( there is a possibility that cell don't even need that high amount of it) they can oxidize. That triggers inflammatory receptors which were show in the video. Then monocytes come and transform into macrophages which are able to "consume" oxidized LDL's and go throught the endothelium. And to take content of LDL back to the bloodflow our body use HDL's throught the egzocytosis. :)
You said: >They are transported through the endocytosis. That makes intracellular cholesterol. So all cells in the body should show an increased cholesterol level internally? That is not where cholesterol is showing up, is it? Intracellularly? Cells use cholesterol for membrane synthesis but only when they "request" it. It doesn't just show up intracellularly and "clog"things up like sugar tends to. Perhaps you are getting the two mechanisms confused.
Well actually in the case of LDL's they move to the cell throught the endocytosis. In the case of macrophages ( I guess that's what you're asking) they use MMP enzymes and katepsins to move throught the basement membrane and to build up between endotelium and miothelium. That's right, foam cells are not inside endothelium cells :)
So then for clarification: Cholesterol in the blood isn't just floating around. It is attached to LDL. Too high of a cholesterol level and cells that are in need of it for cell membrane formation don't present enough of the transport proteins? So the extra cholesterol Oxidizes? Extracellularly? So again, how did it get in to the area behind the intimal lining? Or is it accumulating and oxidizing on the very smooth surface of the intimal lining?I haven't heard of extracellular cholesterol causing a problem? I have heard of normal tears in the cell membrane, especially at larger branching areas, and especially among those with high blood pressure, being inundated with inflamatory cells to clean up the wound....inflammation. What I haven't figured out is why high cholesterol is considered inflammatory and reducing the blood levels does nothing for lowering risk of CVD. ?? Is cholesterol just residue of dying infammatory cells in an area of injury?? Or is it a causative agent?
Yes, it's the content of the LDL's that oxidates and that just triggers inflammation and that process should happen extracellulary on the surface od the first layer. Then monocytes come there transforming into macrophages who "eat" your oxidated LDL's and go throught the first layer of your artery by the help of their own enzymes. And yes, receptors on the cell are a factor here too. If the cell got enough of cholesterol products, she will try to reduce absorbtion of it. Just like a water in the kidneys and closing aquaporines( but here cell just produce less gens responsible for receptor production). High cholesterol is related to inflammation actually because of that property that LDL's can oxidate(specific it's fatty acids, not cholesterol itself, because LDL's contains not only cholesterol. He's just the major here and cuz of him we've got more LDL's. Despite oxidation even the apoproteins of LDL could be changed and provoke macrophages). Less LDL's (containing cholesterol) then less chance for them to stack and oxidate = less chance to cause inflammation. In fact anything than can disturb your endothelium can provoke arterosclerosis, but we are focused on cholesterol because many series of research show that decreasing that value decreased CVD-related deaths and it's value is easier for us to control. BTW arterosclerosis can invoke higher blood pressure because of more narrow space in the artery. And of course cholesterol (and other factors like smoking or even some pharmaceutics) provoke the first step of plaque. Next are joining and proliferation of muscle cells of 2nd layer of artery in the plaque. Proliferation of connective tissue, tearing the 1st layer provoking blood clotting and calcification. I live in a Poland and there is a quacker called Jerzy Zięba. He actually thinks that we should decrease Ca jons to prevent plaque and he believes that cholesterol is totally safe. He blames homocysteine which is of course is a factor, but mostly genetic when cholesterol (as it his higher percentage could be genetic also) is mostly because of diet. Homocysteine should be a problem only when we can't transform it into the metionine with the help of B12 and foliac acid due to deficiency. Decreasing Ca jons could have really bad implications, but whatever...
I came here fro high school to learn about atherosclerosis. Ended up watching a university graduate degree level of the process. I wish information are made simpler :(.
Great Video --> really gives a visual of what is going on. A lot easier to follow then reading out of a textbook :)
It was such an amazing video...really god job ..Thank you
Most welcome 😊
that was great illustration
Thanks
Amazing
❤❤
Thank you!
i love you Craig
The LDL molecules can pass in and out of the intima? What are relative sizes of the LDL and the spaces you are referring to? Certainly they are not entering the cell walls of the intimal cells.
Hello. Not directly, not by itself. They are transported throught the endocytosis. In a normal situation there are special receptors for LDL in the cells which make cholesterol transport into the cell possible. When the acummulation of LDL is so high that your receptors are too slow to absorb all of them ( there is a possibility that cell don't even need that high amount of it) they can oxidize. That triggers inflammatory receptors which were show in the video. Then monocytes come and transform into macrophages which are able to "consume" oxidized LDL's and go throught the endothelium. And to take content of LDL back to the bloodflow our body use HDL's throught the egzocytosis. :)
You said: >They are transported through the endocytosis.
That makes intracellular cholesterol.
So all cells in the body should show an increased cholesterol level internally?
That is not where cholesterol is showing up, is it? Intracellularly? Cells use cholesterol for membrane synthesis but only when they "request" it. It doesn't just show up intracellularly and "clog"things up like sugar tends to.
Perhaps you are getting the two mechanisms confused.
Well actually in the case of LDL's they move to the cell throught the endocytosis. In the case of macrophages ( I guess that's what you're asking) they use MMP enzymes and katepsins to move throught the basement membrane and to build up between endotelium and miothelium. That's right, foam cells are not inside endothelium cells :)
So then for clarification: Cholesterol in the blood isn't just floating around. It is attached to LDL. Too high of a cholesterol level and cells that are in need of it for cell membrane formation don't present enough of the transport proteins? So the extra cholesterol Oxidizes? Extracellularly? So again, how did it get in to the area behind the intimal lining? Or is it accumulating and oxidizing on the very smooth surface of the intimal lining?I haven't heard of extracellular cholesterol causing a problem? I have heard of normal tears in the cell membrane, especially at larger branching areas, and especially among those with high blood pressure, being inundated with inflamatory cells to clean up the wound....inflammation. What I haven't figured out is why high cholesterol is considered inflammatory and reducing the blood levels does nothing for lowering risk of CVD.
?? Is cholesterol just residue of dying infammatory cells in an area of injury?? Or is it a causative agent?
Yes, it's the content of the LDL's that oxidates and that just triggers inflammation and that process should happen extracellulary on the surface od the first layer. Then monocytes come there transforming into macrophages who "eat" your oxidated LDL's and go throught the first layer of your artery by the help of their own enzymes. And yes, receptors on the cell are a factor here too. If the cell got enough of cholesterol products, she will try to reduce absorbtion of it. Just like a water in the kidneys and closing aquaporines( but here cell just produce less gens responsible for receptor production).
High cholesterol is related to inflammation actually because of that property that LDL's can oxidate(specific it's fatty acids, not cholesterol itself, because LDL's contains not only cholesterol. He's just the major here and cuz of him we've got more LDL's. Despite oxidation even the apoproteins of LDL could be changed and provoke macrophages).
Less LDL's (containing cholesterol) then less chance for them to stack and oxidate = less chance to cause inflammation. In fact anything than can disturb your endothelium can provoke arterosclerosis, but we are focused on cholesterol because many series of research show that decreasing that value decreased CVD-related deaths and it's value is easier for us to control. BTW arterosclerosis can invoke higher blood pressure because of more narrow space in the artery. And of course cholesterol (and other factors like smoking or even some pharmaceutics) provoke the first step of plaque. Next are joining and proliferation of muscle cells of 2nd layer of artery in the plaque. Proliferation of connective tissue, tearing the 1st layer provoking blood clotting and calcification.
I live in a Poland and there is a quacker called Jerzy Zięba. He actually thinks that we should decrease Ca jons to prevent plaque and he believes that cholesterol is totally safe. He blames homocysteine which is of course is a factor, but mostly genetic when cholesterol (as it his higher percentage could be genetic also) is mostly because of diet. Homocysteine should be a problem only when we can't transform it into the metionine with the help of B12 and foliac acid due to deficiency. Decreasing Ca jons could have really bad implications, but whatever...
I came here fro high school to learn about atherosclerosis. Ended up watching a university graduate degree level of the process. I wish information are made simpler :(.
try herbal tea remedies that stimulates blood circulation and relief from Atherosclerosis
ruclips.net/video/JGvkYKNApXQ/видео.html
The exact meaning of " cut to the chaise" 👌👏👏👏🌹
Top notch
But the background music is a bit scary
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