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Glucotoxicity promotes aberrant activation and mislocalization of Ras-related C3 botulinum toxin substrate 1 [Rac1] and metabolic dysfunction in pancreatic islet β-cells: Reversal of such metabolic defects by metformin
Emerging evidence suggests that long-term exposure of insulin-secreting pancreatic β-cells to hyperglycemic [HG; glucotoxic] conditions promotes oxidative stress, which, in turn, leads to stress kinase activation, mitochondrial dysfunction, loss of nuclear structure and integrity and cell apoptosis....
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| 出版年: | Apoptosis |
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| 主要な著者: | , , , |
| フォーマット: | Artigo |
| 言語: | Inglês |
| 出版事項: |
2017
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| 主題: | |
| オンライン･アクセス: | https://ncbi.nlm.nih.gov/pmc/articles/PMC5643241/ https://ncbi.nlm.nih.gov/pubmed/28828705 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1007/s10495-017-1409-8 |
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