Reactive oxygen and nitrogen species pathway (ROS/RNS)

The Reactive Oxygen and Nitrogen Species (ROS/RNS) pathway components comprise a complex network of enzymes and molecules responsible for maintaining cellular redox homeostasis [2, 3]. Key enzymatic members include NADPH oxidases (NOX), superoxide dismutases (SOD), catalases, and nitric oxide synthases (NOS), which generate or process reactive intermediates such as superoxide, hydrogen peroxide, and nitric oxide [2, 8]. While these species are vital for normal physiological signaling, including immune defense and vascular tone regulation, their dysregulation leads to oxidative and nitrosative stress [7, 9]. This stress results in cumulative damage to cellular macromolecules like DNA, proteins, and lipids, serving as a driver for chronic diseases such as atherosclerosis, Alzheimer's disease, and various cancers [4, 5]. Pharmacological intervention typically focuses on either neutralizing excess reactive species through scavengers or modulating the activity of specific enzymes and transcription factors, such as Nrf2, to bolster the cell's natural antioxidant defenses [5, 8]. Drugs like N-acetylcysteine and Bardoxolone methyl are used to mitigate oxidative damage, though therapeutic challenges remain regarding the disruption of essential physiological signaling [5, 9]. Monitoring efficacy often involves measuring biomarkers of oxidative damage, such as malondialdehyde or 8-hydroxy-2'-deoxyguanosine [1, 4].

Other names

Reactive oxygen species pathwayReactive nitrogen species pathwayRONS pathwayRedox signaling pathwayOxidative stress pathway

Drugs targeting this pathway act by scavenging free radicals, inhibiting ROS-generating enzymes like NADPH oxidase or xanthine oxidase, or activating transcription factors like Nrf2 to enhance the expression of endogenous antioxidant enzymes.