ATF: Biomed ENG

Takahashi Lab

 
 

Necrotic cell death at physiological extracellular O2 levels in single cardiomyocytes with elevated O2 consumption. Inhibition of creatine kinase accelerated the cell death.

  1. •Takahashi E, Asano K: Mitochondrial respiratory control can compensate for intracellular O2 gradients in cardiomyocytes at low Po2. Am J Physiol 283: H871-H878, 2002.

  2. •Takahashi E: Anoxic cell core can promote necrotic cell death in cardiomyocytes at physiological extracellular Po2. Am J Physiol 294: H2507-H2515, 2008.

Paradoxical necrotic cell death at physiological extracellular O2


We demonstrated a paradox that necrotic cell death can be induced in isolated single cardiomyocytes at physiological oxygen levels (eg, 2-5%) when mitochondrial respiration is stimulated. This cell death was significantly accelerated after inhibition of creatine kinase (CK). Because mitochondrial membrane potential was abolished in the cell core, we concluded that CK mediated energy flux from the cell surface to the cell core may avoid the overall cell death in the presence of anoxic core.

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