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Inflammation and cholesterol

Nilsson, Jan LU ; Ares, Mikko LU ; Lindholm, Marie LU ; Nordin Fredrikson, Gunilla LU and Jovinge, Stefan LU (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:
author
organization
publishing date
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
2007-11-19 16:32:41
date last changed
2016-04-16 04:57:36
@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},
  keyword      = {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},
  volume       = {4},
  year         = {2002},
}