Perivascular adipose tissue (PVAT) is now recognized as a redox-sensitive compartment that modulates vascular homeostasis. In physiological states, PVAT contributes to vascular protection by restraining oxidative stress and preserving nitric oxide bioavailability. Aging disrupts redox balance in PVAT and drives a phenotypic shift marked by mitochondrial dysfunction, increased reactive oxygen species (ROS) generation, and impaired antioxidant defenses. Together, these alterations create a pro-oxidative and pro-inflammatory environment within aged PVAT that impairs endothelial function and promotes vascular remodeling. Against this background, ferroptosis may represent an additional redox-dependent mechanism linking iron dysregulation, lipid peroxidation, and mitochondrial dysfunction in PVAT. Disruption of the GPX4–glutathione antioxidant system may further increase ferroptotic susceptibility and amplify oxidative and inflammatory signaling. This review summarizes current advances in understanding PVAT redox remodeling during aging, with emphasis on redox imbalance and ferroptosis as interconnected mechanisms contributing to PVAT dysfunction and its vascular consequences.