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An Abundant Dysfunctional Apolipoprotein A1 in Human Atheroma

A study performed by a Cleveland Clinic research team and published in Nature Medicine suggests that HDL particle function, rather than size and quantity, contributes to pathophysiological changes seen in the development of atherosclerotic and arteriosclerotic lesions.  Specifically, the Cleveland Clinic team cited the presence of a highly oxidized, dysfunctional, and lipid-poor form of apolipoprotein A1 (ApoA1), the protein component of high density lipoprotein (HDL), in human atheromas.  The study authors demonstrated that myeloperoxidase (MPO) is responsible for the oxidation of HDL, disrupting its ability to serve as a reverse cholesterol transporter, a function conventionally believed to convey HDL’s antiatherosclerotic properties.  Further, this dysfunctional form of ApoA1, oxTrp72-apoA1, demonstrated proinflammatory effects on endothelial cells and impaired HDL formation in vivo.  The authors concluded that “elevated oxTrp72-apoA1 levels in subjects presenting to a cardiology clinic (n = 627) were associated with increased cardiovascular disease risk.” 


Reference:

Huang Y, Didonato JA, Levison BS, et al. An abundant dysfunctional apolipoprotein A1 in human atheroma. Nature medicine. 2014.

 

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