Key result
Mitochondrial nitric oxide synthase (mtNOS) modulation plays a critical role in adapting oxygen uptake, regulating reactive oxygen species, and controlling signaling pathways for proliferation and apoptosis.
Mitochondrial NOS modulation is essential for regulating cellular oxygen uptake, reactive oxygen species production, and signaling pathways involved in cellular adaptation, proliferation, and apoptosis.
mtNOS modulation may influence cardiac bioenergetics and cell survival; leaves open its therapeutic targeting pending clinical studies.
In the last years, nitric oxide synthases (NOS) have been localized in mitochondria. At this site, NO yield directly regulates the activity of cytochrome oxidase, O(2) uptake and the production of reactive oxygen species. Recent studies showed that translocated neuronal nitric oxide synthase (nNOS) is posttranslationally modified including phosphorylation at Ser 1412 (in mice) and myristoylation in an internal residue. Different studies confirm that modified nNOS alpha is the main modulable isoform in mitochondria. Modulation of mtNOS was observed in different situations, like adaptation to reduced O(2) availability and hypoxia, adaptation to low environmental temperature, and processes linked to life and death by effects on kinases and transcription factors. We present here evidence about the role of mtNOS in the analyzed conditions.
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C. Carreras María (2006) reported a review. mtNOS modulation was evaluated. Mitochondrial nitric oxide synthase (mtNOS) modulation plays a critical role in adapting oxygen uptake, regulating reactive oxygen species, and controlling signaling pathways for proliferation and apoptosis.
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