Cellular and Molecular Life Sciences CMLS

, Volume 61, Issue 18, pp 2343–2360

New insight on the molecular mechanisms of high-density lipoprotein cellular interactions

  • L. O. Martinez
  • S. Jacquet
  • F. Tercé
  • X. Collet
  • B. Perret
  • R. Barbaras
Review

DOI: 10.1007/s00018-004-4087-y

Cite this article as:
Martinez, L.O., Jacquet, S., Tercé, F. et al. CMLS, Cell. Mol. Life Sci. (2004) 61: 2343. doi:10.1007/s00018-004-4087-y

Abstract

High-density lipoprotein (HDL) cholesterol is an independent negative risk factor for coronary artery disease and thus represents today the only protective factor against atherosclerosis. The protective effect of HDL is mostly attributed to its central function in reverse cholesterol transport (RCT), a process whereby excess cell cholesterol is taken up and processed in HDL particles, and is later delivered to the liver for further metabolism and bile excretion. This process relies on specific interactions between HDL particles and cells, both peripheral (cholesterol efflux) and hepatic (cholesterol disposal) cells, and on the maturation of HDL particles within the vascular compartment. The plasma level of HDL cholesterol will thus result also from the complex interplay with cellular partners. Among them, some contribute to HDL formation – for instance ATP binding cassette AI protein – while others are mostly involved in HDL catabolism, the scavenger receptor-class B type I or the recently described membrane-bound ATP synthase/hydrolase. The last decade has seen major breakthroughs in the identification and elucidation of the role of cellular partners of HDL metabolism, and in their transcriptional regulations, opening up new perspectives in the modulation of HDL cholesterol.

LipoproteinAtherosclerosisHDLlipoprotein receptorsABCA1 proteinscavenger receptorsF1F0-ATPsynthaseHDL cholesterol

Copyright information

© Birkhäuser-Verlag Basel 2004

Authors and Affiliations

  • L. O. Martinez
    • 1
  • S. Jacquet
    • 1
  • F. Tercé
    • 1
  • X. Collet
    • 1
  • B. Perret
    • 1
  • R. Barbaras
    • 1
  1. 1.Institut Féderatif de Recherche Claude de Preval, IFR 30, Institut National de la Santé et de la Recherche Médicale, Unité 563Centre de Physiopathologie de Toulouse-Purpan, Département Lipoprotéines et Médiateurs LipidiquesToulouse cedexFrance