Age: a modifiable risk factor for cardiovascular disease?

Abstract

Age is the strongest risk factor for cardiovascular disease, yet biological aging is increasingly recognized as a modifiable process. Animal studies over the past few decades have demonstrated that genetic, pharmacological, and dietary interventions can extend the healthspan and lifespan of animals by targeting conserved mechanisms of aging. Examining whether lifespan-extending interventions work in humans is challenging due to the long lifespan of our species. However, the development of biomarkers of biological aging or "aging clocks" has allowed for human trials where the rate of biological aging can be estimated. These surrogate markers now enable the first generation of human geroscience trials, in which interventions such as caloric restriction, rapamycin, taurine, plasma exchange, or nutritional strategies are evaluated for their ability to slow biological aging. Particularly relevant for cardiology are recently developed organ- and cell-specific aging clocks that estimate the biological age of the heart, vasculature, and cardiovascular cell types. These biomarkers may be suitable for improving cardiovascular risk prediction and providing surrogate outcomes for trials targeting cardiovascular aging. Together, these advances suggest that slowing biological aging could complement established cardiovascular prevention and treatment strategies in the future.