Study summary · research use only
Genetically encoded biosensors for evaluating NAD(+)/NADH ratio in cytosolic and mitochondrial compartments
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study (species not specified; conducted in cultured live cells) reports the development of compartment-targeted genetically encoded biosensors, mt-SoNar and ct-SoNar, to monitor the NAD+/NADH ratio in mitochondrial and cytosolic compartments respectively. The abstract reports the fluorescence signal of SoNar responded linearly to physiological NAD+/NADH ratios in situ, that cytosolic and mitochondrial NAD+/NADH ratios responded rapidly but differently to acute metabolic perturbations, indicating distinct NAD pools, and that subcellular NAD redox balance was restored via the malate-aspartate shuttle. Mitochondrial and cytosolic NAD+/NADH ratios were reported to be influenced by NAD+ precursor levels and distinctly regulated under pathophysiological conditions.
Abstract
The ratio of oxidized to reduced NAD (NAD+/NADH) sets intracellular redox balance and antioxidant capacity. Intracellular NAD is compartmentalized and the mitochondrial NAD+/NADH ratio is intricately linked to cellular function. Here, we report the monitoring of the NAD+/NADH ratio in mitochondrial and cytosolic compartments in live cells by using a modified genetic biosensor (SoNar). The fluorescence signal of SoNar targeted to mitochondria (mt-SoNar) or cytosol (ct-SoNar) responded linearly to physiological NAD+/NADH ratios in situ. NAD+/NADH ratios in cytosol versus mitochondria responded rapidly, but differently, to acute metabolic perturbations, indicating distinct NAD pools. Subcellular NAD redox balance regained homeostasis via communications through malate-aspartate shuttle. Mitochondrial and cytosolic NAD+/NADH ratios are influenced by NAD+ precursor levels and are distinctly regulated under pathophysiological conditions. Compartment-targeted biosensors and real-time imaging allow assessment of subcellular NAD+/NADH redox signaling in live cells, enabling future mechanistic research of NAD redox in cell biology and disease development.
pepmg summarizes the peer-reviewed literature and links to every source — it sells nothing, ships nothing, and gives no medical, dosing, or human-use guidance. Don't just trust this summary: follow the citation to its source and read it yourself. Research use only.