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Reactive oxygen species (ROS)-mediated cellular targets refer to a diverse group of molecules, including proteins, lipids, and nucleic acids, that undergo structural or functional changes in response to oxidative modifications [1]. These targets are central to redox signaling, where low levels of ROS act as secondary messengers to regulate processes such as cell growth, differentiation, and immune responses [2]. However, excessive ROS production leads to oxidative stress, causing irreversible damage to these targets and contributing to the pathogenesis of various conditions, including cancer, neurodegeneration, and cardiovascular diseases [3]. Key protein targets include redox-sensitive transcription factors like Nrf2, which orchestrates the antioxidant response, and NF-κB, which regulates inflammation [4]. Therapeutic interventions often aim to modulate these targets using antioxidants or by targeting ROS-producing enzymes like NADPH oxidases (NOX) to restore redox balance [5]. Despite their therapeutic potential, the ubiquitous nature of ROS signaling makes it difficult to target these molecules without interfering with vital physiological functions [6].
Modulation of redox-sensitive signaling pathways, scavenging of reactive species, or inhibition of ROS-generating enzymes such as NADPH oxidase.
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