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Published on: October 12, 2017
High-density lipoprotein metabolism, composition, function, and deficiency
Ernst J Schaefer1, Pimjai Anthanont, Bela F Asztalos
1Lipid Metabolism Section, Cardiovascular Nutrition Laboratory, Human Nutrition Research Center on Aging, Tufts University, Boston, Massachusetts, USA.
Insights
Recent research highlights the crucial role of HDL proteins, including apolipoprotein A-I (apoA-I), myeloperoxidase (MPO), and paraoxonase 1 (PON1), in high-density lipoprotein (HDL) function and coronary heart disease (CHD) risk.
Area of Science:
- Cardiovascular Research
- Lipid Metabolism
- Molecular Biology
Background:
- High-density lipoprotein (HDL) plays a critical role in reverse cholesterol transport and cardiovascular health.
- Understanding HDL composition and function is essential for developing effective strategies against coronary heart disease (CHD).
- Genetic mutations affecting key HDL-related proteins can lead to severe metabolic disorders and premature CHD.
Purpose of the Study:
- To review recent advancements in HDL metabolism, composition, and function.
- To explore the impact of HDL deficiency states caused by genetic mutations.
- To examine the relationship between HDL and coronary heart disease (CHD).
Main Methods:
- Review of current scientific literature on HDL metabolism and function.
- Analysis of genetic studies investigating mutations in apolipoprotein (apo) A-I, ATP-binding cassette transfer protein A1, and lecithin cholesterol acyltransferase (LCAT) genes.
- Examination of the protein complex within HDL, including apoA-I, myeloperoxidase (MPO), and paraoxonase 1 (PON1).
Main Results:
- The HDL complex includes apoA-I, MPO, and PON1, which are critical for HDL binding and function.
- MPO negatively impacts HDL function, while PON1 has a beneficial effect.
- Deficiencies in apoA-I, ATP-binding cassette transfer protein A1, or LCAT lead to premature CHD, hepatosplenomegaly, neuropathy, or kidney failure, with reported heterogeneity.
Conclusions:
- Proteins beyond apoA-I and apoA-II, such as MPO and PON1, significantly influence HDL function.
- Substantial progress has been made in understanding HDL protein content and its functional implications.
- Further research into HDL composition and function may reveal new therapeutic targets for cardiovascular diseases.
Purpose Of Review:
To examine the recent advances in our knowledge of HDL metabolism, composition, function, and coronary heart disease (CHD), as well as marked HDL deficiency states because of mutations in the apolipoprotein (apo) A-I, ATP-binding cassette transfer protein A1 and lecithin cholesterol acyltransferase (LCAT) gene loci.
Recent Findings:
It has been documented that apoA-I, myeloperoxidase and paraoxonase 1 (PON1) form a complex in HDL that is critical for HDL binding and function. Myeloperoxidase has a negative impact on HDL function, whereas PON1 has a beneficial effect. Patients who lack apoA-I develop markedly premature CHD. Patients who lack ATP-binding cassette transfer protein A1 transporter function have only very small discoidal preβ-1 HDL, and develop hepatosplenomegaly, intermittent neuropathy and premature CHD, although significant heterogeneity for these disorders has been reported. Patients with LCAT deficiency have abnormal small discoidal LDLs and HDL particles, and develop kidney failure. Enzyme replacement therapy is being developed for the latter disorder.
Summary:
Recent data indicates that proteins other than apoA-I and apoA-II such as MPO and PON1 have important effects on HDL function. There has been considerable recent progress made in our understanding of HDL protein content and function.
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