Title |
Anti-apoptotic Actions of PPAR-γ Against Ischemic Stroke
|
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Published in |
Molecular Neurobiology, February 2010
|
DOI | 10.1007/s12035-010-8103-y |
Pubmed ID | |
Authors |
Wen-Hsuan Fong, Hsin-Da Tsai, Yu-Chang Chen, Jui-Sheng Wu, Teng-Nan Lin |
Abstract |
Stroke is a leading cause of adult disability and mortality. Diabetes is a major risk factor for stroke. Patients with diabetes have a higher incidence of stroke and a poorer prognosis after stroke. Peroxisome proliferator-activated receptor gamma (PPAR-gamma) is a ligand-modulated transcriptional factor and a therapeutic target for treating type II diabetes. It is well-documented that activation of PPAR-gamma can also attenuate postischemic inflammation and damage. In this review, we focus on the newly revealed anti-apoptotic actions of PPAR-gamma against cerebral ischemia. PPAR-gamma, by increasing superoxide dismutase/catalase and decreasing nicotinamide adenine dinucleotide phosphate oxidase levels, attenuated ischemia-induced reactive oxygen species and subsequently alleviated the postischemic degradation of Bcl-2, Bcl-xl, and Akt. The preserved Akt phosphorylated Bad. Meanwhile, PPAR-gamma also promotes the transcription of 14-3-3epsilon. Elevated 14-3-3epsilon binds and sequesters p-Bad and prevents Bad translocation to neutralize the anti-apoptotic function of Bcl-2. This review further supports the notion that PPAR-gamma may serve as a potential therapeutic target for treating ischemic stroke. |
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Geographical breakdown
Country | Count | As % |
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Unknown | 45 | 100% |
Demographic breakdown
Readers by professional status | Count | As % |
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Student > Ph. D. Student | 10 | 22% |
Student > Master | 9 | 20% |
Researcher | 7 | 16% |
Student > Bachelor | 5 | 11% |
Student > Doctoral Student | 3 | 7% |
Other | 3 | 7% |
Unknown | 8 | 18% |
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Other | 6 | 13% |
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