Reactive oxygen species and redox-sensitive pathways (ROS/Redox pathways)

Reactive oxygen species (ROS) and redox-sensitive pathways represent a complex network of oxygen-derived molecules and the signaling systems that respond to changes in cellular reduction-oxidation (redox) states. These molecules, including superoxide anions and hydrogen peroxide, act as essential signaling mediators in physiological processes such as cell proliferation and immune activation [PubMed: 28236004]. Under normal conditions, redox homeostasis is maintained by a balance between ROS generation and antioxidant defense systems like the Nrf2 pathway [PubMed: 25911333]. Pathological oxidative stress occurs when this balance is disrupted, leading to oxidative damage to cellular components and contributing to diseases like cancer, atherosclerosis, and Alzheimer's [PubMed: 21402143]. Therapeutic interventions target these pathways through various mechanisms, including direct scavenging of ROS or the pharmacological induction of endogenous antioxidant enzymes. Drugs like N-acetylcysteine and dimethyl fumarate are used to modulate these pathways in clinical settings for conditions ranging from acetaminophen toxicity to multiple sclerosis. However, the broad and essential nature of redox signaling presents significant challenges, as excessive suppression of ROS can interfere with vital physiological functions. Consequently, modern drug development focuses on site-specific or context-dependent modulation of redox-sensitive nodes to achieve therapeutic efficacy without systemic toxicity.

Other names

Oxidative stress pathwaysRedox signalingReactive oxygen speciesRedox-sensitive signaling cascades

Modulation of redox homeostasis through direct scavenging of reactive species, inhibition of ROS-generating enzymes such as NADPH oxidase (NOX), or pharmacological activation of antioxidant transcription factors like Nrf2 to enhance endogenous defenses [PubMed: 25911333].