Neuropathic pain is a chronic and debilitating condition characterized by persistent neuroinflammation, oxidative stress, and neuronal sensitization. Increasing experimental evidence indicates that nuclear factor erythroid 2–related factor 2 (NRF2), a master regulator of cellular antioxidant responses, plays a protective role in neuropathic pain by modulating redox homeostasis and inflammatory signaling pathways. Pharmacological activation of NRF2 attenuates mechanical hypersensitivity in preclinical models through induction of cytoprotective genes such as HO-1 and NQO1 and suppression of pro-inflammatory cascades. Beyond its mechanistic relevance, NRF2 signaling represents a promising framework for the development of molecular biomarkers and translational strategies aimed at improving diagnostic precision and therapeutic targeting in neuropathic pain. Although clinical validation remains limited, current evidence supports further investigation of redox-regulated pathways as potential diagnostic and therapeutic tools in chronic pain disorders.
Pérez-Leal et al. (Sun,) studied this question.