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Isolation of High-density Lipoproteins for Non-coding Small RNA Quantification
Published on: November 28, 2016
High-Density Lipoprotein Function and Dysfunction in Health and Disease
Scott T Chiesa1, Marietta Charakida2,3
1Vascular Physiology Unit, UCL Institute of Cardiovascular Science, 1 St. Martin's Le Grand, London, EC1A 4NP, UK. s.chiesa@ucl.ac.uk.
Insights
High-density lipoprotein cholesterol (HDL-c) may not be protective against cardiovascular disease (CVD). HDL
Area of Science:
- Cardiovascular Science
- Lipid Metabolism
- Inflammation Biology
Background:
- High-density lipoprotein cholesterol (HDL-c) traditionally termed 'good cholesterol' shows an inverse relationship with cardiovascular disease (CVD) risk.
- Recent genetic studies and randomized controlled trials challenge HDL-c's causal role in cardiovascular protection.
- Emerging research shifts focus from HDL-c levels to the functional properties of HDL particles.
Purpose of the Study:
- To review the relationship between HDL and CVD risk.
- To explore how chronic inflammation alters HDL composition and function.
- To discuss potential therapeutic interventions targeting HDL.
Main Methods:
- Literature review of genetic studies.
- Analysis of large-scale randomized controlled trials.
- Examination of evidence on HDL composition and function in inflammatory conditions.
Main Results:
- Evidence suggests HDL-c levels do not causally protect against CVD.
- HDL particle composition and function are altered in inflammatory states.
- Altered HDL may transition from a protective to a pro-atherogenic particle.
Conclusions:
- The protective role of HDL against CVD is questionable.
- Inflammation significantly impacts HDL functionality, potentially promoting atherosclerosis.
- Future therapies may focus on modulating HDL function rather than just increasing levels.
Abstract:
High-density lipoprotein cholesterol (HDL-c) has long been referred to as 'good cholesterol' due to its apparent inverse relationship with future CVD risk. More recent research has questioned a causal role for HDL-c in this relationship, however, as both genetic studies and numerous large-scale randomised controlled trials have found no evidence of a cardiovascular protective effect when HDL-c levels are raised. Instead, focus has switched to the functional properties of the HDL particle. Evidence suggests that both the composition and function of HDL may be significantly altered in the context of an inflammatory milieu, transforming the particle from a vasoprotective anti-atherogenic particle to a noxious pro-atherogenic equivalent. This review will summarise evidence relating HDL to CVD risk, explore recent evidence characterising changes in the composition and function of HDL that may occur in chronic inflammatory diseases, and discuss the potential for future HDL-modifying therapeutic interventions.
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