Autophagy is a highly regulated process involving the removal of damaged proteins and organelles from cells and tissues through a lysosomal-mediated pathway. Accumulating evidence suggests that autophagy is necessary to maintain redox homeostasis. Here, we explore the connection between autophagy and reactive oxygen species (ROS). In particular, we discuss how oxidant-dependent signaling can modulate autophagic flux and how autophagy can, in turn, modulate ROS levels. Finally, we discuss how a decline or disruption of autophagy might contribute to redox-dependent cardiovascular pathology and help fuel the age-dependent decline in cardiovascular function.