Inflammation and cholesterol
(2002) In European Heart Journal Supplements 4(Suppl A). p.18-25- Abstract
- Atherosclerosis develops as a result of a chronic arterial inflammation and intimal Fibrosis. The disease represents in many respects a vascular repair process activated in response to injury caused by toxic breakdown products of aggregated and oxidized lipoproteins. The initial response of the artery involves expression of adhesion molecules and recruitment of leukocytes. Degenerated lipoproteins are removed front the extracellular space by macrophages. If lipoproteins continue to I process becomes chronic and accumulate. the inflammatory cytokines stimulate smooth muscle to migrate into the intima. These cells proliferate and form an atherosclerotic plaque. Plaque cell death and inflammation in response to oxidized lipids and other toxic... (More)
- Atherosclerosis develops as a result of a chronic arterial inflammation and intimal Fibrosis. The disease represents in many respects a vascular repair process activated in response to injury caused by toxic breakdown products of aggregated and oxidized lipoproteins. The initial response of the artery involves expression of adhesion molecules and recruitment of leukocytes. Degenerated lipoproteins are removed front the extracellular space by macrophages. If lipoproteins continue to I process becomes chronic and accumulate. the inflammatory cytokines stimulate smooth muscle to migrate into the intima. These cells proliferate and form an atherosclerotic plaque. Plaque cell death and inflammation in response to oxidized lipids and other toxic factors May Cause plaques to rupture. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/343894
- author
- Nilsson, Jan LU ; Ares, Mikko LU ; Lindholm, Marie LU ; Nordin Fredrikson, Gunilla LU and Jovinge, Stefan LU
- organization
- publishing date
- 2002
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- lipoproteins, atherosclerosis, macrophages, immunity, smooth muscle, cells
- in
- European Heart Journal Supplements
- volume
- 4
- issue
- Suppl A
- pages
- 18 - 25
- publisher
- Oxford University Press
- external identifiers
-
- wos:000173748600003
- ISSN
- 1520-765X
- language
- English
- LU publication?
- yes
- id
- ea98341a-9638-44ae-a2cb-0f4964b12c4c (old id 343894)
- alternative location
- http://eurheartjsupp.oxfordjournals.org/cgi/reprint/4/suppl_A/A18
- date added to LUP
- 2016-04-01 16:50:19
- date last changed
- 2018-11-21 20:44:36
@article{ea98341a-9638-44ae-a2cb-0f4964b12c4c, abstract = {{Atherosclerosis develops as a result of a chronic arterial inflammation and intimal Fibrosis. The disease represents in many respects a vascular repair process activated in response to injury caused by toxic breakdown products of aggregated and oxidized lipoproteins. The initial response of the artery involves expression of adhesion molecules and recruitment of leukocytes. Degenerated lipoproteins are removed front the extracellular space by macrophages. If lipoproteins continue to I process becomes chronic and accumulate. the inflammatory cytokines stimulate smooth muscle to migrate into the intima. These cells proliferate and form an atherosclerotic plaque. Plaque cell death and inflammation in response to oxidized lipids and other toxic factors May Cause plaques to rupture.}}, author = {{Nilsson, Jan and Ares, Mikko and Lindholm, Marie and Nordin Fredrikson, Gunilla and Jovinge, Stefan}}, issn = {{1520-765X}}, keywords = {{lipoproteins; atherosclerosis; macrophages; immunity; smooth muscle; cells}}, language = {{eng}}, number = {{Suppl A}}, pages = {{18--25}}, publisher = {{Oxford University Press}}, series = {{European Heart Journal Supplements}}, title = {{Inflammation and cholesterol}}, url = {{http://eurheartjsupp.oxfordjournals.org/cgi/reprint/4/suppl_A/A18}}, volume = {{4}}, year = {{2002}}, }