Abstract
Elastin is a key elastomeric protein responsible for the elasticity of many organs, including heart, skin, and blood vessels. Due to its intrinsic long life and low turnover rate, damage induced by pathophysiological conditions, such as hyperglycemia and medial elastocalcinosis, chronologically accumulate during aging. Evidence has shown that hyperglycemia triggers tissue damage and loss of mechanical functions of elastin via the accumulation of advanced glycation end products (AGEs). Medial elastocalcinosis, on the other hand, has not only been demonstrated to deteriorate the function of aortic tissues, but also has been speculated to be facilitated by elevated glucose levels.
Published Version
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