Genetic variants predisposing to cardiovascular disease

Abstract

During the last year, tremendous effort has been made in elucidating new genes associated with cardiovascular disease predisposition. For the most part, however, major breakthroughs have not been made, primarily due to the poor replication of results among studies, as a consequence of poor experimental design. Nevertheless, we have increased our understanding of the complexity of cardiovascular disease and the relevance of gene-environment interactions as the ultimate drivers of the individual predisposition to the disease. It is essential, therefore, that present and future genetic studies in this area take into consideration the inclusion of high-quality environmental data in the analytical process to test the clinical usefulness of a genetic marker as a risk predictor.

Class IIa histone deacetylases: regulating the regulators

“…It is now essential to establish whether alterations of the class IIa HDAC-MEF2 axis occur in these human pathologies. Genetic alterations of MEF2 family members have been linked to cardiovascular diseases (Wang, 2005;Visvikis-Siest and Marteau, 2006) and acute lymphoblastic leukemia (Yuki et al, 2004;Prima et al, 2005). Similarly, alterations of MEF2 transcriptional activity have been implicated in neurodegenerative disorders (Camins et al, 2006) and cardiac hypertrophy (Czubryt and Olson, 2004).…”

Apolipoprotein E Gene Polymorphism And Its Effect On Plasma Lipids In Arteriosclerosis

“…For decades, Apo E has been regarded as one of the important factor of lipoprotein genetics [9,10]. Several studies have demonstrated the impact of Apo E polymorphisms in cerebrovascular and cardiovascular diseases in a reproducible fashion.…”

Spontaneous Atherosclerosis in Pigeons: A Good Model of Human Disease

“…These interactions have made it difficult to establish a universally accepted mechanism of atherogenesis (Peltonen & McKusick, 2001), because the sample sizes needed to test these gene-gene and gene-environment interactions are much larger than those needed for simpler genotype-phenotype associations (Ordovas & Shen, 2002). Pathways that trigger atherosclerosis in the general population have yet to be elucidated (Visvikis-Siest & Marteau, 2006). Most genomic scale experiments have compared either full-blown plaques against non-affected aortic segments (Archacki et al, 2003;Forcheron et al, 2005;Hiltunen et al, 2002;Shanahan et al, 1997), or they have analyzed differences between ruptured and unruptured plaques (Adams et al, 2006;Faber et al, 2001;Papaspyridonos et al, 2006).…”

“…Markers do not necessarily cause the disease, but can be used to improve diagnosis and risk assessment (Gibbons et al, 2004). Inflammatory markers such as C-reactive protein (CRP) factors [Tsimikas et al, 2006;Ridker, 2000] plus markers of oxidative damage such as myeloperoxidase (Shao et al, 2006) and paraoxanase (Visvikis-Siest & Marteau, 2006) have already increased clinicians' predictive power. As more markers of atherosclerosis are correlated with disease progression and outcome, the genetic variation contributing to predisposition and initial manifestation will become clear.…”