Autophagy and Proteostasis in Cardiac Aging

Autophagy is a homeostatic process to maintain healthy macromolecules within cells through the degradation and turnover of damaged or defective cellular components. Autophagic function declines with age, in parallel with the development of several degenerative diseases, including cardiac aging. Cardiac aging is an intrinsic process of slowly progressive changes in molecules and cells leading to cardiac dysfunction. These degenerative changes are closely associated with a decline in quality control mechanisms. This chapter discusses the role of autophagy and protein homeostasis (proteostasis) in aging, provides a general overview of the manifestation of cardiac aging, and the mechanisms involved in maintaining homeostasis and retarding cardiac aging. While focusing on autophagy, we also review other interrelated mechanisms: mitochondrial oxidative damage and quality control and ubiquitin-proteasomal system. Interventions known to delay aging and cardiovascular diseases are discussed in relationship to autophagy, including calorie restriction, rapamycin, resveratrol, and mitochondrial protective treatments.