Aging, Smooth Muscle Vitality, and Aortic Integrity
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Advances in medical genetics and imaging have resulted in a significant increase in the number of diagnosed thoracic aortic aneurysms (TAA). Recent findings establish a link between diminished nicotinamide phosphoribosyltransferase (NAMPT) and compromised smooth muscle cell vitality in aortic dilatation. These findings have myriad implications given the diverse roles of NAMPT, which is central to the production of nicotinamide adenine dinucleotide (NAD+) and, thus, ATP production, as well the activity of multiple NAD+ consuming proteins. Given its central role in vascular cell vitality and, thus, matrix integrity, further attention should be directed to the NAMPT–NAD+ control system in thoracic aortopathy.
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Aging is a primary risk factor for many cardiovascular diseases. The manifold effects of vascular aging result, in part, from adverse phenotypic changes to endothelial cells and vascular smooth muscle cells (VSMCs), increased inflammation, and associated changes in extracellular matrix (ECM) composition, structure, and mechanical properties.1 These aging-related changes progress in different ways throughout the vasculature. Aging of the aorta manifests at the vessel level as a gradual dilatation and structural stiffening, which impact the global hemodynamics and local wall mechanics. In particular, a stiffer aorta increases the pulse wave velocity, which can augment the pulse pressure in the proximal (thoracic) aorta and increase mechanical stress. Increases in mechanical loading are typically sensed by the VSMCs and result in changes in gene expression and downstream gene products that affect the composition and structure of the aortic wall, thus establishing a feedback loop connecting mechanical loading, cell function, and structural integrity.2
In addition to genetic mutations and uncontrolled hypertension, aging is an important risk factor for the development of TAAs. Defined as a ≥50% dilatation of the aorta, these lesions are characterized histopathologically by damaged elastic fibers, compromised smooth muscle function, pooled …