Reactive oxygen species and oxidative stress cascade (ROS) (ROS)

The reactive oxygen species (ROS) and oxidative stress cascade is a complex biological process involving the generation of highly reactive oxygen-containing molecules and the subsequent cellular response. ROS, including superoxide, hydrogen peroxide, and hydroxyl radicals, are primarily produced as byproducts of mitochondrial respiration or by specialized enzymes like NADPH oxidases (NOX) [1, 2]. Under physiological conditions, ROS act as vital signaling molecules in processes such as vascular tone regulation and immune response; however, an imbalance between ROS production and antioxidant defense leads to oxidative stress [3]. This state results in oxidative damage to DNA, proteins, and lipids, contributing to the pathogenesis of numerous chronic conditions, including Alzheimer's disease, atherosclerosis, and various cancers [2, 3]. Therapeutic strategies targeting this cascade include the use of direct antioxidants, Nrf2 activators to boost endogenous defenses, and specific inhibitors of ROS-generating enzymes [4]. Despite the clear role of oxidative stress in disease, clinical success has been limited by the challenge of targeting pathological ROS without interfering with essential redox signaling [1].

Other names

Oxidative stress pathwayRedox signaling cascadeReactive oxygen species signalingOxidative damage cascade

Drugs modulate this cascade by directly scavenging reactive species, inhibiting ROS-producing enzymes (e.g., NADPH oxidase), or activating the Nrf2-Keap1 pathway to induce endogenous antioxidant enzymes like superoxide dismutase and glutathione peroxidase [1, 2].