Apolipoprotein A-I mimetic peptides

Curr Atheroscler Rep. 2009 Jan;11(1):52-7. doi: 10.1007/s11883-009-0008-8.


Recent publications reveal the mechanism of action of apolipoprotein A-I (apoA-I) mimetic peptides to be the remarkable binding affinity that oxidized lipids have for these peptides compared with apoA-I. There was no difference in the binding affinity of oxidized lipids or in peptide efficacy in reducing inflammation and atherosclerosis in rabbits injected with peptides synthesized from all D- or all L-amino acids. The apoA-I mimetic peptide 4F increased the formation of pre-beta high-density lipoprotein, increased cholesterol efflux, and reduced lipoprotein oxidation in vitro; it increased antioxidants and vascular repair in type 1 diabetic rats; it improved vasodilation, oxidative stress, myocardial inflammation, and angiogenic potential in a mouse model of scleroderma; it reduced renal inflammation in low-density lipoprotein receptor-null mice fed a Western diet; it reduced arthritis in a rat model; it reduced adiposity, increased adiponectin levels, and improved insulin sensitivity in obese mice; and it improved high-density lipoprotein inflammatory properties in humans with coronary heart disease.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Anti-Inflammatory Agents / pharmacology
  • Anti-Inflammatory Agents / therapeutic use
  • Apolipoprotein A-I / pharmacology*
  • Apolipoprotein A-I / therapeutic use*
  • Arthritis / drug therapy
  • Atherosclerosis / prevention & control
  • Cholesterol, HDL / blood
  • Diabetes Mellitus / drug therapy
  • Disease Models, Animal
  • Humans
  • Hyperlipidemias / complications
  • Nephritis / drug therapy
  • Nephritis / etiology
  • Obesity / drug therapy
  • Scleroderma, Systemic / drug therapy


  • Anti-Inflammatory Agents
  • Apolipoprotein A-I
  • Cholesterol, HDL