Advanced glycation end-products (AGEs) are a form of metabolic byproduct that build up with age, causing increasing damage through their effects on cellular machinery, which ultimately manifest in harmful conditions such as reduced elasticity in blood vessels and skin. Ways to safely break down the most important forms of AGE would be greatly beneficial - but research aimed at achieving that goal is unfortunately very sparse and poorly funded.
Here researchers show that some of the mechanisms of heart failure and decline in heart function correlate with the level of AGEs in the body:
Aging is accompanied by increased vascular and ventricular stiffness, diastolic dysfunction and an increased risk of heart failure. Heart failure, with either reduced or preserved ejection fraction, is associated with abnormalities of myocardial structure and microvasculature including increased fibrosis, cardiomyocyte hypertrophy and reduced microvascular density, and animal models suggest that these abnormalities precede the development of heart failure in older age.
In addition, advanced glycation end-products (AGEs) are proposed to contribute to the increased myocardial stiffening of aging by cross-linking collagen and elastin and promoting collagen accumulation, and by promoting inflammation and oxidative stress mediated by the receptor for AGEs (RAGE). Moreover, plasma AGE levels correlate with the severity and prognosis of heart failure and predict all-cause and cardiovascular disease mortality in older adults.
We investigated the hypothesis that diastolic dysfunction of aging humans is associated with altered myocardial structure and plasma AGE levels. [We found that] diastolic dysfunction of aging was independent of myocardial structure but was associated with plasma AGE levels.