The environment, epigenetic landscape and cardiovascular risk

Cardiovascular disease (CVD) is the most common non-communicable disease worldwide. Future projections predict an increasing CVD burden due to aging, urbanization, and unhealthy lifestyles with devastating socio-economic implications in emerging countries. Despite implementation of traditional risk score models and state-of-the-art treatment strategies, CVD is far from being eradicated. Atherothrombosis underlies the majority of CV events and mostly develops from unforeseeable disruption of atheromatous plaque with subsequent platelet activation and thrombus formation. This condition is triggered by the derail of molecular pathways involved in oxidative stress, inflammatory changes and endothelial dysfunction. CV risk phenotype is extremely heterogeneous and the development/progression of CVD depends on aging, environmental, and genetic factors.1 However, gene –environment interaction only partially explains the phenotypic variability of CV risk, suggesting that other mechanisms play an important role. In this perspective, a growing body of evidence supports the notion that epigenetics variations, linking the environment to long-lasting effects on the p henotype, are a key mechanism of increased CV risk (Figure 1).

Source: Cardiovascular Research - June 23, 2019 Category: Cardiology Source Type: research