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Hypoxia in murine atherosclerotic plaques and its adverse effects on macrophages

Saj Parathath1, Yuan Yang, Stephanie Mick

  • 1Department of Medicine (Cardiology), Marc and Ruti Bell Program in Vascular Biology, NYU School of Medicine, Smilow 7, 522 First Ave., New York, NY 10016, USA.

Trends in Cardiovascular Medicine
|February 5, 2013
PubMed

Insights

Hypoxia, or low oxygen, is confirmed in mouse models of atherosclerosis. This condition impacts lipid synthesis and cholesterol transport, with HIF-1α playing a key role.

Area of Science:

  • Cardiovascular Biology
  • Atherosclerosis Research
  • Hypoxia Studies

Background:

  • Hypoxia is present in human atherosclerotic plaques.
  • The occurrence of hypoxia in mouse models of atherosclerosis has been debated due to their small size.

Purpose of the Study:

  • To review evidence confirming hypoxia in apolipoprotein E-deficient (apoE-/-) mouse models.
  • To explore the in vitro effects of hypoxia on lipid metabolism and cholesterol efflux.
  • To investigate the role of HIF-1α in mediating these hypoxic effects.

Main Methods:

  • Review of a recent report on hypoxia detection in apoE-/- mouse plaques.
  • In vitro experiments assessing lipid synthesis and cholesterol efflux.
  • Analysis of the involvement of the transcription factor HIF-1α.

Main Results:

  • Direct evidence of hypoxia was found in atherosclerotic plaques of apoE-/- mice.
  • In vitro, hypoxia increased lipid synthesis and decreased cholesterol efflux via the ABCA1 pathway.
  • HIF-1α mediated a significant portion, but not all, of these hypoxia-induced changes.

Conclusions:

  • Hypoxia is demonstrable in mouse models of atherosclerosis, validating their use in research.
  • Hypoxia influences key cellular processes in atherosclerosis, including lipid metabolism and cholesterol transport.
  • Findings provide insights into the pathophysiology of atherosclerosis and potential therapeutic targets.

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