Nutrient excess and altered mitochondrial proteome and function contribute to neurodegeneration in diabetes.
Nutrient excess and altered mitochondrial proteome and function contribute to neurodegeneration in diabetes.
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DOI:
10.1016/j.mito.2011.06.007
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发表时间:
2011-11
期刊:
影响因子:
4.4
通讯作者:
Femyhough, Paul
中科院分区:
文献类型:
--
作者:
Chowdhury, Subir K. Roy;Dobrowsky, Rick T.;Femyhough, Paul
Diabetic neuropathy is a major complication of diabetes that results in the progressive deterioration of the sensory nervous system. Mitochondrial dysfunction has been proposed to play an important role in the pathogenesis of the neurodegeneration observed in diabetic neuropathy. Our recent work has shown that mitochondrial dysfunction occurs in dorsal root ganglia (DRG) sensory neurons in streptozotocin (STZ) induced diabetic rodents. In neurons, the nutrient excess associated with prolonged diabetes may trigger a switching off of AMP kinase (AMPK) and/or silent information regulator T1 (SIRT1) signaling leading to impaired peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α expression/activity and diminished mitochondrial activity. This review briefly summarizes the alterations of mitochondrial function and proteome in sensory neurons of STZ-diabetic rodents. We also discuss the possible involvement of AMPK/SIRT/PGC-1α pathway in other diabetic models and different tissues affected by diabetes.
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影响因子:
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作者:
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通讯作者:
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DOI:
10.1523/jneurosci.3347-10.2011
发表时间:
2011-02-02
期刊:
The Journal of neuroscience : the official journal of the Society for Neuroscience
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DOI:
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发表时间:
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影响因子:
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作者:
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通讯作者:
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影响因子:
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作者:
Handschin, Christoph;Chin, Sherry;Spiegelman, Bruce M.
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