HDL metabolism, composition, function and deficiency #MMPMID24785961
Schaefer EJ; Anthanont P; Asztalos BF
Curr Opin Lipidol 2014[Jun]; 25 (3): 194-9 PMID24785961show ga
Purpose of review: Our purpose was to examine recent advances in our knowledge of high density lipoprotein (HDL) metabolism, composition, function, and coronary heart disease (CHD), as well as marked HDL deficiency states due to mutations at the apolipoprotein (apo) A-I, ATP binding cassette transfer protein A1 (ABCA1), and lecithin cholesterol acyltransferase (LCAT) gene loci. Recent findings: It has been documented that apoA-I, myeloperoxidase (MPO), and paraoxonase 1 (PON1) form a complex in HDL that is critical for HDL binding and function. MPO has a negative impact on HDL function, while PON1 has a beneficial effect. Patients that lack apoA-I develop markedly premature CHD. Patients that lack ABCA1 transporter function have only very small discoidal pre?-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 low density lipoproteins 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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Curr+Opin+Lipidol 2014 ; 25 (3): 194-9
