title: The role of hypoxia in atherosclerosis.
abstract: OBJECTIVE
  It is important to address the factors involved in the progression of atherosclerosis because advanced atherosclerotic lesions are prone to rupture, leading to disability or death. Hypoxic areas are known to be present in human atherosclerotic lesions, and lesion progression is associated with the formation of lipid-loaded macrophages and increased local inflammation. Here we summarize the role of hypoxia in the development of advanced atherosclerotic lesions by promoting lipid accumulation, inflammation, ATP depletion, and angiogenesis.
  
  
  RESULTS
  A recent study clearly demonstrated the presence of hypoxia in macrophage-rich regions of advanced human carotid atherosclerotic lesions. We showed that hypoxia increases the formation of lipid droplets in macrophages and promotes increased secretion of inflammatory mediators, and recent evidence indicates that lipid droplets may play a role in mediating the inflammatory response. Hypoxia also promotes lesion progression by exacerbating ATP depletion and lactate accumulation, and the presence of hypoxia in human carotid atherosclerotic lesions correlates with angiogenesis.
  
  
  CONCLUSIONS
  Recent studies indicate that hypoxia may play a key role in the progression to advanced lesions by promoting lipid accumulation, increased inflammation, ATP depletion, and angiogenesis. Further understanding of the effects of hypoxia in atherosclerotic lesions could indicate potential therapeutic targets.
authors: Sahlgrenska Center for Cardiovascular and Metabolic Research, Wallenberg Laboratory, University of Gothenburg, Sweden. Lillemor.Mattsson@wlab.gu.se
authors: Lillemor Mattsson
authors: LM
authors: Hultén
authors: Max
authors: M
authors: Levin
mesh_terms: D000818:Animals; D050197:Atherosclerosis / Q000150:complications* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D005487:Foam Cells / Q000378:metabolism; D006801:Humans; D000860:Hypoxia / Q000150:complications* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D007249:Inflammation / Q000150:complications; D009389:Neovascularization, Pathologic / Q000209:etiology