A range of processes are involved in age-related stiffening of blood vessel walls. Cross-linking in the extracellular matrix leads to a loss of elasticity, as does disruption of elastin structures. In addition, inflammation and other issues cause dysfunction in the vascular smooth muscle cells responsible for contraction and dilation. Stiffness leads to hypertension, which in turn causes structural damage to delicate tissues throughout the body. Thus there is a strong incentive to better understand why stiffening occurs, and identify which of the various processes are most important and most amenable to interventions that might reverse this aspect of aging.
Arterial stiffness (AS) is one of the earliest detectable signs of structural and functional alterations of the vessel wall and an independent predictor of cardiovascular events and death. The emerging field of metabolomics can be utilized to detect a wide spectrum of intermediates and products of metabolism in body fluids that can be involved in the pathogenesis of AS. Research over the past decade has reinforced this idea by linking AS to circulating acylcarnitines, glycerophospholipids, sphingolipids, and amino acids, among other metabolite species.
Some of these metabolites influence AS through traditional cardiovascular risk factors (e.g., high blood pressure, high blood cholesterol, diabetes, smoking), while others seem to act independently through both known and unknown pathophysiological mechanisms. We propose the term 'arteriometabolomics' to indicate the research that applies metabolomics methods to study AS. The 'arteriometabolomics' approach has the potential to allow more personalized cardiovascular risk stratification, disease monitoring, and treatment selection. One of its major goals is to uncover the causal metabolic pathways of AS. Such pathways could represent valuable treatment targets in vascular ageing.