Autophagy is an essential cellular pathway by which protein aggregates, long-lived proteins, or defective organelles are sequestered in double membrane vesicles and then degraded upon fusion of those vesicles with lysosomes. Although autophagy plays a critical role in maintaining intracellular homeostasis and keeping the cell in a healthy state, this key pathway can become dysregulated in various cardiometabolic disorders, such as; obesity, dyslipidemia, inflammation, and insulin resistance. In these conditions, autophagy may actually worsen the pathological state instead of protecting the cell or organism. In this review, we discuss how dysregulated autophagy may be linked to increases in cardiovascular risk factors, and how manipulation of the autophagic machinery might reduce those risks.