Role for Mitochondrial Oxidants as Regulators of Cellular Metabolism

We further demonstrate that in turn, the redox-dependent activation of JNK1 feeds back and inhibits the activity of the metabolic enzymes glycogen synthase kinase 3β and glycogen synthase

Shino Nemoto


Scholarcy highlights

  • Leakage of mitochondrial oxidants contributes to a variety of harmful conditions ranging from neurodegenerative diseases to cellular senescence
  • The burst of tyrosine phosphorylation stimulated by platelet-derived growth factor or epidermal growth factor is significantly attenuated by overexpression of the peroxide-scavenging enzyme catalase
  • An increase in mitochondrial reactive oxygen species develops as a consequence of the increase in metabolism, and the subsequent generation of H2O2 is essential for the activation of JNK1
  • Pyruvate causes a fall in GSK-3␤ activity. This reduction in GSK-3␤ activity requires the redoxdependent activation of JNK1 and appears to proceed through RSK3 activation
  • The largest increase in JNK1 activity came at a high pyruvate concentration, suggesting that the pathways described here may primarily operate in the setting of a sudden, large increase in metabolic supply
  • This is consistent with our observations that under conditions in which pyruvate stimulated JNK1 activity, both mitochondrial and cytosolic ROS levels rose

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