Properly developed large elastic arteries serve as reservoirs that store stroke volume during systole and damp downstream blood pressure fluctuations. This function is enabled by the extracellular matrix (ECM) protein elastin. Mouse gene expression data reveals that elastin expression begins during embryonic development and peaks around postnatal day (P) 14. Expression then decreases to low levels for the remainder of adult life, indicating that elastin production during development is critical for a properly functioning vessel [1]. Reduced elastin in humans due to genetic mutations is associated with a congenital narrowing of the ascending aorta, known as supravalvular aortic stenosis, and chronic hypertension [2].

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