ArticleeLife2021
A coarse-grained NADH redox model enables inference of subcellular metabolic fluxes from fluorescence lifetime imaging.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 25 citations in OpenAlex.
- Early Postmortem Changes in NADH Fluorescence Lifetime Parameters in Rat Skeletal Muscle: Potential for Postmortem Interval Estimation.International journal of molecular sciences · 2026Article
- Control theory analysis of dynamic metabolic response elucidates mitochondrial-cytoplasmic coupling and nutrient partitioning.bioRxiv : the preprint server for biology · 2026Article
- Energetic gradients emerge in developing motor-microtubule structures.bioRxiv : the preprint server for biology · 2026Article
- Article
- Imaging mitochondrial membrane potential via concentration-dependent fluorescence lifetime changes.Nature communications · 2025Article
- Development of Cellular Energy Metabolism During Differentiation of Human iPSCs into Cortical Neurons.Molecular neurobiology · 2025Article
- Redox-dependent binding and conformational equilibria govern the fluorescence decay of NAD(P)H in living cells.FEBS letters · 2025Article
- Thermodynamic dissipation constrains metabolic versatility of unicellular growth.Nature communications · 2025Article
- Advanced strategies for single embryo selection in assisted human reproduction: A review of clinical practice and research methods.Clinical and experimental reproductive medicine · 2025Article
- Energy partitioning in the cell cortex.Nature physics · 2024Article
- Robustness of mitochondrial biogenesis and respiration explain aerobic glycolysis.bioRxiv : the preprint server for biology · 2024Article
- Historic obstacles and emerging opportunities in the field of developmental metabolism - lessons from Heidelberg.Development (Cambridge, England) · 2024Review
- Metabolic imaging of human cumulus cells reveals associations with pregnancy and live birth.Human reproduction (Oxford, England) · 2024Observational
- Visualizing subcellular changes in the NAD(H) pool size versus redox state using fluorescence lifetime imaging microscopy of NADH.Communications biology · 2024Article
- Spatial patterning of energy metabolism during tissue morphogenesis.Current opinion in cell biology · 2023Review
- A molecular rotor FLIM probe reveals dynamic coupling between mitochondrial inner membrane fluidity and cellular respiration.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Noninvasive metabolic profiling of cumulus cells, oocytes, and embryos via fluorescence lifetime imaging microscopy: a mini-review.Human reproduction (Oxford, England) · 2023Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial metabolism is of central importance to diverse aspects of cell and developmental biology. Defects in mitochondria are associated with many diseases, including cancer, neuropathology, and infertility. Our understanding of mitochondrial metabolism in situ and dysfunction in diseases are limited by the lack of techniques to measure mitochondrial metabolic fluxes with sufficient spatiotemporal resolution. Herein, we developed a new method to infer mitochondrial metabolic fluxes in living cells with subcellular resolution from fluorescence lifetime imaging of NADH. This result is based on the use of a generic coarse-grained NADH redox model. We tested the model in mouse oocytes and human tissue culture cells subject to a wide variety of perturbations by comparing predicted fluxes through the electron transport chain (ETC) to direct measurements of oxygen consumption rate. Interpreting the fluorescence lifetime imaging microscopy measurements of NADH using this model, we discovered a homeostasis of ETC flux in mouse oocytes: perturbations of nutrient supply and energy demand of the cell do not change ETC flux despite significantly impacting NADH metabolic state. Furthermore, we observed a subcellular spatial gradient of ETC flux in mouse oocytes and found that this gradient is primarily a result of a spatially heterogeneous mitochondrial proton leak. We concluded from these observations that ETC flux in mouse oocytes is not controlled by energy demand or supply, but by the intrinsic rates of mitochondrial respiration.
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