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- W128216279 abstract "In summary, it is clear that hypoxia promotes pulmonary artery constriction via the activation of a “metabolic sensor(s)” and a “primary effector(s)”. The “primary effector” may then modulate a variety of other cell functions associated with HPV, including cADPR accumulation. Hypoxia likely triggers these events by inhibiting oxidative phosphorylation by mitochondria, leading to an increase in cytoplasmic AMP levels as the adenylate kinase reaction seeks to maintain ATP levels. I propose that a build up of AMP leads to the activation of the primary “metabolic sensors/primary effectors” in O2-sensing cells, namely AMPK kinase and AMPK, respectively, and that AMPK, in addition to promoting glucose uptake and anaerobic glycolysis, may activate ADP-ribosyl cyclase and cADPR accumulation by hypoxia. Subsequently, increased β-NADH formation by anaerobic glycolysis may augment cADPR accumulation. As the severity of hypoxia increases, however, β-NADH levels may increase still further, leading to a consequent fall in cADPR levels due to reduced substrate availability (β-NAD+), and ultimately to the failure of maintained HPV (Fig. 5). While, I cannot rule out the possibility that a paradoxical increase in mitochondrial ROS by hypoxia may also promote cADPR accumulation, this seems unlikely." @default.
- W128216279 created "2016-06-24" @default.
- W128216279 creator A5040302772 @default.
- W128216279 date "2006-02-22" @default.
- W128216279 modified "2023-09-25" @default.
- W128216279 title "Hypoxia, Cell Metabolism, and cADPR Accumulation" @default.
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- W128216279 doi "https://doi.org/10.1007/1-4020-7858-7_18" @default.
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