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Oxidative stress and programmed cell death in diabetic neuropathy
Andrea M Vincent1, Michael Brownlee, James W Russell
1Department of Neurology, University of Michigan, Ann Arbor, Michigan 48109, USA.
Annals of the New York Academy of Sciences
|April 27, 2002
Summary
Diabetic neuropathy involves oxidative stress, mitochondrial dysfunction, and cell death. Therapies targeting reactive oxygen species (ROS) may effectively treat this condition by protecting neurons and Schwann cells.
Area of Science:
- Neuroscience
- Cell Biology
- Diabetology
Background:
- Oxidative stress, mitochondrial membrane depolarization (MMD), and programmed cell death (PCD) are linked to diabetic neuropathy.
- Hyperglycemia in diabetic rats causes neuronal and Schwann cell mitochondrial damage, mirroring findings in human sural nerve biopsies.
Purpose of the Study:
- To investigate the role of oxidative stress and mitochondrial dysfunction in diabetic neuropathy.
- To explore therapeutic strategies targeting reactive oxygen species (ROS) and mitochondrial integrity.
Main Methods:
- Utilized streptozotocin (STZ)-treated diabetic rats and human sural nerve biopsies.
- Examined mitochondrial changes, ROS production, and caspase activation in neurons and Schwann cells exposed to high glucose.
- Assessed the efficacy of interventions like growth factors (NGF) and uncoupling proteins (UCPs).
Main Results:
- High glucose increased ROS production and induced MMD, leading to caspase activation and PCD in neurons and Schwann cells.
- Mitochondrial swelling and cristae disruption were observed in diabetic models and human neuropathy.
- NGF, reduced ROS generation, and UCP up-regulation inhibited PCD by stabilizing mitochondrial membrane potential.
Conclusions:
- Hyperglycemia-induced oxidative stress drives neuronal and Schwann cell death in diabetic neuropathy.
- Targeting ROS production and stabilizing mitochondrial function represent promising therapeutic avenues for diabetic neuropathy.