Stress-induced adaptive islet cell identity changes.
Stress-induced adaptive islet cell identity changes.
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DOI：
10.1111/dom.12726
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发表时间：
2016-09
期刊：
影响因子：
--
通讯作者：
Herrera PL
中科院分区：
文献类型：
--
作者：
Cigliola V;Thorel F;Chera S;Herrera PL
不同形式的糖尿病的发病机制不同，但最终，它们都以进行性胰岛β细胞损失为特征。因此，恢复β细胞团是未来治疗方法的主要目标。出生时发现的β细胞数量由胰腺祖细胞的增殖和分化决定，并且被认为在整个成年生活中基本保持不变。最近在小鼠中的研究揭示了胰岛内分泌细胞对应激的反应具有意想不到的可塑性;在某些条件下，胰岛非β细胞具有重新编程为胰岛素生产者的潜力，从而有助于恢复β细胞群。本文主要讨论了在生理、病理和实验应激条件下胰腺和胰岛细胞可塑性的最新研究成果。了解这些模型中细胞重编程的机制将允许通过利用胰腺的内在再生能力来开发治疗糖尿病的新策略。
The different forms of diabetes mellitus differ in their pathogenesis but, ultimately, they are all characterized by progressive islet β-cell loss. Restoring the β-cell mass is therefore a major goal for future therapeutic approaches. The number of β-cells found at birth is determined by proliferation and differentiation of pancreatic progenitor cells, and it has been considered to remain mostly unchanged throughout adult life. Recent studies in mice have revealed an unexpected plasticity in islet endocrine cells in response to stress; under certain conditions, islet non-β-cells have the potential to reprogram into insulin producers, thus contributing to restore the β-cell mass. Here, we discuss the latest findings on pancreas and islet cell plasticity upon physiological, pathological and experimental conditions of stress. Understanding the mechanisms involved in cell reprogramming in these models will allow the development of new strategies for the treatment of diabetes, by exploiting the intrinsic regeneration capacity of the pancreas.
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