Cells need a continuous energy supply to function, but making ATP is only part of the story. We measure mitochondrial respiration and the routes that carry energy within cells, helping distinguish limited energy production from a problem with energy delivery or use.
What we can measure
- Mitochondrial respiratory capacity. Use high-resolution respirometry to measure oxygen consumption and the capacity of the mitochondrial energy-producing system.
- Response to metabolic inputs. Control substrates and ADP concentrations to determine how a cell's energy system responds to changing demand.
- Metabolic and redox state. Monitor NADH autofluorescence alongside respiration to follow changes in cellular metabolism in real time.
- Intracellular energy transfer. Quantify how ATP and ADP move between mitochondria and the parts of the cell that use energy, including the effect of diffusion barriers and local enzyme coupling.
How we work
We design measurements around the biological question, using intact or permeabilized cells under carefully controlled conditions. By combining respirometry, fluorescence measurements, enzyme assays, and mathematical models, we turn complex metabolic traces into an interpretable account of energy production and transfer.
Questions this can answer
- Is a reduced cellular function caused by lower mitochondrial capacity or by impaired energy delivery?
- Does a compound change how mitochondria respond to energetic demand or metabolic substrates?
- Are ATP and ADP able to move effectively between energy-producing and energy-using parts of the cell?
- Do disease models alter the organisation or coupling of the enzymes that support cellular energy transfer?
Experience
Our laboratory has a long record of studying how cardiac cells match energy supply to demand. We have used respiration, NADH autofluorescence, enzyme measurements, and quantitative models to show how cellular structure and local metabolic coupling shape energy transfer. This experience helps us identify the mechanism behind an altered metabolic readout rather than reporting a change in oxygen consumption alone.
Selected publications: Branovets et al. (2023), Birkedal et al. (2022), Branovets et al. (2021), Vendelin et al. (2020), Karro et al. (2019), Karro et al. (2017), Simson et al. (2016), Branovets et al. (2013), Jepihhina et al. (2011), and Sepp et al. (2010).