title: Lipoprotein(a): from molecules to therapeutics.
abstract: Lipoprotein (a) [Lp(a)] was discovered by Kare Berg in 1963 from the study of low-density lipoprotein genetic variants. Lp(a) contains a unique protein, apolipoprotein(a), which is linked to the Apo B-100 through a disulfide bond that gives it a great structural homology with plasminogen, and confers it atherogenic and atherothrombotic properties. Interest in Lp(a) has increased because an important association between high plasma levels of Lp(a) and coronary artery disease and cerebral vascular disorders has been demonstrated. Numerous case control studies have confirmed that hyper-Lp(a) is a risk factor for premature cardiovascular disease. Lp(a) is identified as a genetic trait with autosomal transmission, codified by one of the most studied polymorphic genes in humans. It has been demonstrated that variations in this gene are a major factor in the serum levels of Lp(a). Variations differ considerably between individuals and sex across populations. Various approaches to drug treatment using fibric acid derivatives, growth hormone, insulin-like growth factor-1, alcohol extracted soy protein, niacin, and exercise have been proven to decrease Lp(a) in high risk patients, but none has really been an effective therapeutic option for successfully reducing Lp(a) plasma levels.
authors.affiliation: Endocrine and Metabolic Diseases Research Center, University of Zulia, School of Medicine, Maracaibo, Venezuela. valmore@gmail.com
authors.forename: Valmore
authors.initials: V
authors.lastname: Bermúdez
authors.forename: Nailet
authors.initials: N
authors.lastname: Arráiz
authors.forename: Daniel
authors.initials: D
authors.lastname: Aparicio
authors.forename: Edward
authors.initials: E
authors.lastname: Rojas
authors.forename: Daniela
authors.initials: D
authors.lastname: Gotera
authors.forename: Xavier
authors.initials: X
authors.lastname: Guerra
authors.forename: Roger
authors.initials: R
authors.lastname: Canelón
authors.forename: Judith
authors.initials: J
authors.lastname: Faría
authors.forename: Luis
authors.initials: L
authors.lastname: Sorell
authors.forename: Anilsa
authors.initials: A
authors.lastname: Amell
authors.forename: Nadia
authors.initials: N
authors.lastname: Reyna
authors.forename: Mayela
authors.initials: M
authors.lastname: Cabrera
authors.forename: Edgardo
authors.initials: E
authors.lastname: Mengual
authors.forename: Raquel
authors.initials: R
authors.lastname: Cano
authors.forename: Clímaco
authors.initials: C
authors.lastname: Cano
authors.forename: Manuel
authors.initials: M
authors.lastname: Velasco
mesh_terms: D002318:Cardiovascular Diseases / Q000209:etiology / Q000517:prevention & control*; D002561:Cerebrovascular Disorders / Q000209:etiology / Q000517:prevention & control; D003324:Coronary Artery Disease / Q000209:etiology / Q000517:prevention & control; D005260:Female; D006801:Humans; D006951:Hyperlipoproteinemias / Q000150:complications* / Q000188:drug therapy; D017270:Lipoprotein(a) / Q000097:blood* / Q000187:drug effects / Q000235:genetics; D008297:Male; D011110:Polymorphism, Genetic; D012307:Risk Factors
chemical_list: D017270:Lipoprotein(a)