Year: 1990
Type: article
Abstract: I n 1963, Kare Berg 1 immunized rabbits with human low density lipoprotein (LDL) and identified a genetic variation in the anti-LDL antibody response.He attributed this genetic variation to a unique fraction of LDL that he termed lipoprotein(a) (Lp[a]), and he believed that this trait was transmitted in an autosomal dominant fashion.Over the subsequent two decades, data obtained from several groups 2 -6 demonstrated that elevated serum levels of Lp(a) correlate with an increased risk of atherosclerotic vascular disease.The mechanism(s) by which Lp(a) confers this increased risk has eluded identification; however, recent observations on the unique structural features of Lp(a) shed light on some possible explanations for its atherogenic potential and highlight its pathophysiologic role at the interface of atherosclerosis and thrombosis.
Author: J Loscalzo
Institution: Brigham and Women's Hospital
Language: English
Subfield: Cardiology and Cardiovascular Medicine
Field: Medicine
Domain: Health Sciences
Open Access status: diamond
OpenAlex ID: W1998010052