PCSK9 GENE PARTICIPATES IN THE DEVELOPMENT
OF PRIMARY DYSLIPIDEMIAS
Matías-Pérez D1, Pérez-Santiago AD1, Sánchez Medina MA1, Alpuche Osorno JJ2, García-Montalvo IA1
*Corresponding Author: Dr. Iván A. García-Montalvo, Division of Postgraduate Studies and Research,
Tecnológico Nacional de México/Instituto Tecnológico de Oaxaca, Oaxaca City, Oaxaca, México. Av.
Víctor Bravo Ahuja No. 125, Esq. Calzada Tecnológico Oaxaca, Oaxaca. Tel./Fax: +52-951-501-5016.
E-mail: ivan.garcia@itoaxaca.edu.mx
page: 5
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Abstract
Dyslipidemias are a group of diseases, which are characterized
by abnormal blood concentrations of cholesterol,
triglycerides and/or low-density lipoprotein-cholesterol
(LDL-c). Dyslipidemia is a determinant condition for the
progress of an atherosclerotic plaque formation. The resulting
atherogenicity is due to at least two mechanisms: first,
to the accumulation in the plasma of lipid particles that
have the capacity to alter the function of the endothelium
and deposit at the atheromatous plaque, and second, at an
insufficient concentration of multifactorial type of high
density lipoprotein-cholesterol (HDL-c), whose function
is to protect against the development of atherosclerosis. Its
highest prevalence is encountered among individuals with
diabetes, hypertension or overweight. Hyperlipidemia is
one of the main predisposing factors for the development
of cardiovascular disease. Hyperlipidemia can be the result
of a genetic condition, the secondary expression of a
primary process or the consequence of exogenous factors
(food, cultural, socio-economic, etc.), all of which lead to
the elevation of plasma lipid levels. The objective of this
study was to carry out an analysis of the genes involved
in the development of dyslipidemias that lead to cardiovascular
disease with special emphasis on the proprotein
convertase subtilin/kexin type 9 (PCSK9) gene. The
PCSK9 gene participates in the development of primary
dyslipidemias, mainly familial hypercholesterolemia, currently
the pharmacological treatment of choice to reduce
LDL-c are statins, however, it has been observed that these
have been insufficient to eliminate cardiovascular risk,
especially in subjects with primary forms of hypercholesterolemia
related to genetic mutations, or statin intolerance.
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