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过氧化物酶体增殖物激活受体 γ:全身性代谢性疾病与良性前列腺增生之间的分子联系。

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

机构信息

Department of Urologic Surgery, Vanderbilt University Medical Center, Nashville, TN 37232, USA.

出版信息

Differentiation. 2011 Nov-Dec;82(4-5):220-36. doi: 10.1016/j.diff.2011.05.008. Epub 2011 Jun 8.

DOI:10.1016/j.diff.2011.05.008
PMID:21645960
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3174339/
Abstract

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.

摘要

代谢综合征的紧急流行及其一系列复杂的后果要求我们更全面地了解系统性代谢疾病背景下的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,研究了它作为 LUTS 的一个组成部分的作用,并回顾了将 BPH/LUTS 与 2 型糖尿病、炎症和血脂异常联系起来的回顾性临床研究。过氧化物酶体增殖物激活受体 γ(PPARγ)信号通路通过调节炎症和胰岛素抵抗,位于系统性代谢疾病和 BPH/LUTS 的交汇点,被提议作为针对 BPH/LUTS 的分子操作的候选。最后,我们介绍了正在用于研究肥胖、糖尿病和炎症对良性前列腺生长影响的新的细胞和动物模型。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98d5/3174339/6a98abdcb0fa/nihms300054f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98d5/3174339/783671e13d55/nihms300054f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98d5/3174339/c0d41fc421a4/nihms300054f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98d5/3174339/fc31d5bfd852/nihms300054f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98d5/3174339/4d1005284544/nihms300054f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98d5/3174339/6a98abdcb0fa/nihms300054f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98d5/3174339/783671e13d55/nihms300054f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98d5/3174339/c0d41fc421a4/nihms300054f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98d5/3174339/fc31d5bfd852/nihms300054f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98d5/3174339/4d1005284544/nihms300054f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/98d5/3174339/6a98abdcb0fa/nihms300054f5.jpg

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本文引用的文献

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Am J Physiol Endocrinol Metab. 2011 Jan;300(1):E164-74. doi: 10.1152/ajpendo.00219.2010. Epub 2010 Oct 19.
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Statin use and decreased risk of benign prostatic enlargement and lower urinary tract symptoms.
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PPARγ2 functions as a tumor suppressor in a translational mouse model of human prostate cancer.过氧化物酶体增殖物激活受体 γ2 在人前列腺癌的翻译小鼠模型中作为肿瘤抑制因子发挥作用。
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Upregulated PPARG2 facilitates interaction with demethylated AKAP12 gene promoter and suppresses proliferation in prostate cancer.上调的 PPARG2 促进与去甲基化的 AKAP12 基因启动子相互作用,并抑制前列腺癌的增殖。
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