Autophagy is a collection of processes that remove damaged and unwanted molecules and structures from a cell, delivering them to a lysosome where they are broken down into raw materials for further protein synthesis. Many of the approaches shown to slow aging in short-lived species are characterized by improved autophagy, and evidence from research into calorie restriction suggests that autophagy may be the most important of the many mechanisms linking the operation of cellular metabolism to the pace of aging. Autophagy is known to falter with age, and the research community has identified numerous specific defects that arise in older individuals. So far progress has been slow when it comes to the development of therapies that specifically target and improve autophagy, though most calorie restriction mimetic drugs, such as mTOR inhibitors, do so to some degree as a part of their broad effects on metabolism.
We know that the world's population is currently living longer. This is especially problematic, given the increase in the prevalence of chronic conditions resulting from an increased aging population, thus negatively affecting the healthspan and quality of life of the affected individuals. This review discussed the effects of aging on the cardiovascular system and established an increased predisposition of cardiovascular pathologies in the geriatric population due to molecular, structural, and functional changes in both the cardiac and vascular systems. Longevity molecular pathways exist to maintain the homeostasis of the cardiovascular system and promote health. Autophagy is at the interlink of these pathways.
Although autophagy is downregulated as people age, stimulation of this pathway through caloric restriction, intermittent fasting, and supplementation of pharmacologic agents can reinstate autophagy in older individuals. Induced autophagy promotes the longevity of cardiovascular health, thereby instigating the role of autophagy in the prevention of chronic conditions such as cardiovascular ailments. Strong evidence for this notion has emerged from studies using genetically modified mice defective in genes, transcription factors, and proteins essential for autophagy and as such failed to show improvements in cardiovascular health when caloric restriction, intermittent fasting, and pharmacologic agents are implemented.
To summarize, future research should be directed toward human studies or human tissues in vitro. This will allow for a clearer understanding of the role of autophagy on the longevity pathways and cardiovascular disease prevention in humans. In addition, future research should evaluate how the beneficial effects of autophagy can be implemented reproducibly and on large scales in the population.