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. Author manuscript; available in PMC: 2015 Aug 5.
Published in final edited form as: Curr Vasc Pharmacol. 2015;13(4):433–440. doi: 10.2174/1570161112666141014144829

Figure 1. Schematic description of contributions from the interplay between genetic and environmental factors to the development of vascular disease and the role of relative biomarkers in clinical vascular disease phenotypes.

Figure 1

The color spectrum of development of clinical phenotype of vascular disease schematically shows that in most cases the vascular disease is caused neither solely by genomic factors (green) nor totally by environmental (red) factors. The clinical phenotypes of vascular disease in an individual patient are usually a sum result of the complex of interplay between genetic and environmental contributions. Although in some conditions patients with a positive genetic susceptibility to vascular disease may have a major genetic component, whether the patient will manifest the full clinical phenotypes of the vascular disease is dependent on the contributing environmental factors. Conversely, patients may have different thresholds of an environmentally induced vascular disease depending on the individual’s genetic background. A variety of biomarkers (including genes, microRNAs, proteins, small molecules of metabolites, and imaging) can be deployed to delineate disease progression in vascular disease. Genetic biomarkers (gene mutations, single-nucleotide polymorphisms, microRNAs etc.) can identify an individual’s genetic predisposition. However, it is the environmental imprints on the genetic background that are responsible for the dynamic production of abnormal unique proteins and/or small metabolites that foster disease progression in the susceptible individuals. The environmental prediction of vascular disease can be detected using protein or metabolite biomarkers. As the disease progresses further in the susceptible individual, vascular structural and functional alterations can be detected through imaging technologies.