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Published on: October 12, 2017
The role of dysfunctional HDL in atherosclerosis
Mohamad Navab1, Srinivasa T Reddy, Brian J Van Lenten
1Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA 90095-1679, USA. mnavab@mednet.ucla.edu
Insights
Dysfunctional high-density lipoprotein (HDL) impairs reverse cholesterol transport and promotes inflammation, particularly in atherosclerosis. ApoA-I mimetic peptides show promise in restoring HDL function by binding oxidized lipids.
Area of Science:
- Cardiovascular Science
- Lipid Metabolism
- Inflammation Biology
Background:
- High-density lipoprotein (HDL) plays a crucial role in lipid metabolism and possesses anti-inflammatory properties.
- Dysfunctional HDL is implicated in chronic inflammatory conditions, notably atherosclerosis.
- Loss of HDL's anti-inflammatory function often parallels impaired reverse cholesterol transport.
Purpose of the Study:
- To review the role of HDL in regulating low-density lipoprotein (LDL) oxidation and LDL-induced inflammation.
- To explore the mechanisms underlying HDL dysfunction in inflammatory diseases.
- To discuss potential therapeutic strategies for restoring HDL function.
Main Methods:
- Literature review of studies on HDL function, LDL oxidation, and inflammation.
- Analysis of data from animal models and human studies of atherosclerosis.
- Examination of the effects of apoA-I mimetic peptides on HDL function.
Main Results:
- Dysfunctional HDL is associated with increased LDL oxidation and inflammation in atherosclerosis.
- Impaired reverse cholesterol transport is a hallmark of dysfunctional HDL.
- ApoA-I mimetic peptides demonstrate potential in improving HDL function by targeting oxidized lipids.
Conclusions:
- HDL dysfunction contributes significantly to the pathogenesis of atherosclerosis.
- Restoring HDL's anti-inflammatory and cholesterol-efflux capacities is a key therapeutic goal.
- ApoA-I mimetic peptides represent a promising therapeutic avenue for managing HDL dysfunction.
Abstract:
This review focuses on HDL function in modulating LDL oxidation and LDL-induced inflammation. Dysfunctional HDL has been identified in animal models and humans with chronic inflammatory diseases including atherosclerosis. The loss of antiinflammatory function correlated with a loss of function in reverse cholesterol transport. In animal models and perhaps in humans, dysfunctional HDL can be improved by apoA-I mimetic peptides that bind oxidized lipids with high affinity.
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