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The "Reactive oxygen species-related pathway" refers to a collection of cellular processes involving reactive oxygen species (ROS)—highly reactive molecules derived from molecular oxygen such as superoxide anion (O2-), hydrogen peroxide (H2O2), hydroxyl radical (OH.), and singlet oxygen. These molecules arise naturally during aerobic metabolism—primarily in mitochondria—and through specific enzymatic reactions including those catalyzed by NADPH oxidases. At physiological levels, ROS serve essential roles as second messengers regulating signal transduction pathways that control cell proliferation, differentiation, apoptosis, autophagy, immune responses, stem cell maintenance/regeneration, metabolic adaptation, and tissue repair. However, excessive accumulation leads to oxidative stress causing damage to DNA/proteins/lipids—a key driver in aging processes and diseases such as cancer, cardiovascular disorders (atherosclerosis/stroke), diabetes mellitus/metabolic syndrome complications, neurodegeneration/inflammation. The "ROS-related pathway" is not a single molecular target but rather encompasses multiple interconnected biochemical routes including NF-kB/MAPK/PI3K-Akt/Keap1-Nrf2 axis among others that mediate both beneficial adaptive responses ("oxidative eustress") and pathological effects ("oxidative distress"). Therapeutic strategies often focus on modulating these pathways using antioxidants or enzyme inhibitors but must balance maintaining physiological redox homeostasis with preventing harmful oxidative damage.
Drugs may act by scavenging reactive oxygen species directly (antioxidants), inhibiting their production via enzyme inhibition (e.g., NADPH oxidase inhibitors), or activating endogenous antioxidant defense systems through transcription factor modulation (e.g., Nrf2 activators).
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