{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nA broad spectrum of studies has firmly established that NADPH oxidases—particularly the gp91phox‐containing (Nox2) complexes—serve as central regulators of reactive oxygen species (ROS) production. These enzymes are shown to mediate redox‐sensitive signaling, modulate inflammatory responses, and contribute to structural and functional alterations in tissues ranging from the central nervous system and heart to the vasculature and immune system. For example, NADPH oxidase activation has been implicated in ketamine‐induced psychosis, stretch‐induced ROS production in cardiomyocytes, proatherogenic macrophage activation by oxidized low‐density lipoprotein, and maladaptive cardiac remodeling after ischemic insult or pressure overload. In addition, these studies highlight diverse roles for NADPH oxidase–dependent ROS in triggering downstream effectors such as NF‑κB, modulating cytokine expression, and even influencing neural regeneration and antigen processing."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "41"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nNotably, however, a review of the provided literature reveals no direct mention or functional characterization of MIR3714. Although microRNAs frequently act as modulators of gene expression in redox regulation and inflammatory pathways, none of these abstracts evaluate or implicate MIR3714 in the modulation of NADPH oxidase subunits, ROS generation, or the cellular responses elicited by oxidative stress. 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