ReviewMedical gas research2027
Nitric oxide signaling and mitophagy in Parkinson's disease: implications for aerobic exercise-related neuroprotection.
Review in Medical gas research, 2027. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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2 authors.
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Abstract
Parkinson's disease is strongly associated with mitochondrial dysfunction and impaired mitochondrial quality control, including defective mitophagy. Aerobic exercise is increasingly recognized as a safe and accessible intervention that can improve motor and non-motor outcomes in Parkinson's disease and may also engage mechanisms relevant to disease modification. In this review, we propose a context-dependent framework in which aerobic exercise reshapes nitric oxide signaling toward a more adaptive profile, characterized by relatively moderate, transient, and spatially restricted nitric oxide bioactivity, and we discuss how this shift may influence mitochondrial biogenesis, mitophagy initiation, and autophagic flux regulation. Rather than treating nitric oxide as uniformly protective or deleterious, we argue that its biological effects in Parkinson's disease depend on source, concentration, duration, subcellular localization, cellular target, and surrounding redox milieu. However, direct evidence that exercise-derived nitric oxide activates these pathways in Parkinson's disease-relevant neural tissue is still limited. We further highlight major translational gaps, including cell-type and brain-region heterogeneity, incomplete definition of exercise dose-response relationships, and the lack of validated in vivo biomarkers of neuronal mitophagy and nitric oxide dynamics in patients with Parkinson's disease. Overall, aerobic exercise is a plausible modulator of mitophagy-related pathways in Parkinson's disease, and nitric oxide is a credible contributor to this effect; however, the current evidence supports a multi-node, context-dependent model rather than a simple linear mechanism.
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