PPARγ: a molecular link between systemic metabolic disease and benign prostate hyperplasia.

PPARγ: a molecular link between systemic metabolic disease and benign prostate hyperplasia.
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DOI:
10.1016/j.diff.2011.05.008
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发表时间:
2011-11
期刊:
影响因子:
2.9
通讯作者:
Hayward, Simon W.
Hayward, Simon W.
中科院分区:
生物学3区
文献类型:
--
作者:
Jiang, Ming;Strand, Douglas W.;Franco, Omar E.;Clark, Peter E.;Hayward, Simon W.

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代谢综合征的流行及其复杂的后遗症列表要求在全身性代谢疾病的背景下更深入地了解良性前列腺增生和下尿路症状(BPH/LUTS)。在这里,我们讨论了BPH的性质和起源,检查其作为LUTS的一个组成部分的作用,并回顾回顾性临床研究,得出BPH/LUTS和II型糖尿病,炎症和血脂异常之间的关联。PPARγ信号通过调节炎症和胰岛素抵抗而处于全身性代谢疾病和BPH/LUTS的联系中,被认为是BPH/LUTS的分子操纵的候选者。最后,我们介绍了新的细胞和动物模型,用于研究肥胖,糖尿病和炎症对良性前列腺生长的影响。
The emergent epidemic of metabolic syndrome and its complex list of sequelae mandate a more thorough understanding of benign prostatic hyperplasia and lower urinary tract symptoms (BPH/LUTS) in the context of systemic metabolic disease. Here we discuss the nature and origins of BPH, examine its role as a component of LUTS and review retrospective clinical studies that have drawn associations between BPH/LUTS and type II diabetes, inflammation and dyslipidemia. PPARγ signaling, which sits at the nexus of systemic metabolic disease and BPH/LUTS through its regulation of inflammation and insulin resistance is proposed as a candidate for molecular manipulation in regard to BPH/LUTS. Finally, we introduce new cell and animal models that are being used to study the consequences of obesity, diabetes and inflammation on benign prostatic growth.
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