{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nNeuronal nitric‐oxide synthase (NOS1) plays a central role in the central nervous system, where it contributes to neurotransmission, synaptic plasticity, and neurodevelopment. Genetic association studies have linked regulatory variants in NOS1 with major neuropsychiatric disorders such as schizophrenia, bipolar disorder, and even aspects of personality and attention‐deficit hyperactivity disorder. In addition, proper NOS1 expression is critical for early cortical development, as evidenced by FMRP‐mediated translation of NOS1 in specific pyramidal neurons—a finding relevant to fragile X syndrome and cognitive dysfunction. These observations collectively point to a key function for NOS1 in modulating brain circuitry and behavior."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "10"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn the vasculature, NOS1‐derived nitric oxide is essential for regulating basal microvascular tone and ensuring proper regional blood flow. Unlike endothelial NOS‐derived nitric oxide that mediates receptor‐stimulated vasodilatation, NOS1 modulates local vessel tone under resting conditions and during centrally mediated stimuli such as mental stress and whole‐body heat stress. Its activity has been demonstrated in the coronary, forearm, and cutaneous circulations, underscoring the enzyme’s distinct and nonredundant role in cardiovascular homeostasis."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "11", "end_ref": "17"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn skeletal muscle, NOS1 is a key mediator of exercise‐induced signaling. Proper sarcolemmal localization of NOS1 has been shown to support fatigue resistance following mild exercise challenges, and its expression uniformly increases across different muscle fiber types during intense training. These functions contribute to improved endurance and protection against disproportionate fatigue responses."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "18"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn contexts of pathological stress, aberrant NOS1 expression and activity can drive deleterious signaling. Upregulation of NOS1 in cancer‐associated fibroblasts, for instance, sustains protumorigenic functions and promotes lymphangiogenesis, while in mast cells, NOS1 regulates the release of inflammatory mediators such as leukotrienes. Moreover, in models of neurotoxicity, increased NOS1 activity leads to S‐nitrosylation of critical proteins and induction of apoptosis, and in the heart, NOS1 dysregulation has been implicated in altered Ca²⁺ handling that may contribute to heart failure. Finally, under oxidative stress conditions, uncoupling of NOS1—due to shifts in cofactor availability—promotes the formation of reactive oxygen species rather than nitric oxide, thereby exacerbating cellular injury."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "20", "end_ref": "25"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nGenetic and post‐transcriptional regulation further fine‐tunes NOS1 function in peripheral tissues. Alternative splicing events within its 5′‐untranslated region serve as potent regulators of its translation, and polymorphisms in NOS1 have been associated with variations in biomarkers such as exhaled nitric oxide in asthmatic individuals. In addition, NOS1-dependent signaling has been linked to red blood cell function during aging. 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