Live·Open questions in longevity research

Metabolism and energy

Mitochondrial proton leak

Proton passage across the inner mitochondrial membrane that increases oxygen consumption relative to ATP production

Hypotheses on this target 1

Mitochondrial proton leakInhibition. Hypotheses on this target 11Activation. Hypotheses on this target 0Function preservation. Hypotheses on this target 0Supplementation. Hypotheses on this target 0Feedback restoration. Hypotheses on this target 0Direct measurement. Hypotheses on this target 0
  • Inhibition1
  • Activation
  • Function preservation
  • Supplementation
  • Feedback restoration
  • Direct measurement

Inhibition1

  • Mitochondrial proton leakage may make kidney transport consume oxygen inefficiently

    Where this hypothesis actsMitochondria of vulnerable downstream renal tubular cells after SGLT2 blockade

    What is proposedReduce excess proton leak to restore coupling of respiration and ATP synthesis

    With whatNot stated in the record

    HowCorrect the molecular source of the leak after identifying it, while preserving distal reabsorption; the specific intervention is not stated

    Possible resultPossible restoration of tissue oxygenation and reserve, stabilization of SPV_9 and reduced renal contribution to decline

    2026-09-30