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良性前列腺增生的分子与细胞发病机制

Molecular and cellular pathogenesis of benign prostatic hyperplasia.

作者信息

Lee Keith L, Peehl Donna M

机构信息

Department of Urology, Stanford University School of Medicine, Stanford, California 94305-5118, USA.

出版信息

J Urol. 2004 Nov;172(5 Pt 1):1784-91. doi: 10.1097/01.ju.0000133655.71782.14.

Abstract

PURPOSE

Symptomatic benign prostatic hyperplasia (BPH) is one of the most common ailments seen by the urologist. Significant advances have occurred in medical and surgical therapy, and in the understanding of the biology of this disease. However, the basic science literature is often conflicting and confusing, without a unified voice. We report the current state of knowledge of the molecular and cellular basis of BPH.

MATERIALS AND METHODS

We compiled and interpreted basic science studies relevant to BPH pathogenesis.

RESULTS

Cellular alterations that include changes in proliferation, differentiation, apoptosis and senescence in the epithelium and stroma are implicated in BPH pathogenesis. Molecular analyses have yielded numerous candidate genes important in disease progression. Differential expression of cytokines and growth factors in BPH tissue suggests roles for inflammation and hypoxia. Through the use of cell culture models the complex regulatory mechanisms of growth control in BPH are becoming defined.

CONCLUSIONS

The scientific endeavor has resulted in great strides in our understanding of BPH on a molecular and cellular level. It is hopeful that basic science and translational research will improve treatment and prevention strategies for this common disease of elderly men.

摘要

目的

有症状的良性前列腺增生(BPH)是泌尿科医生最常诊治的疾病之一。在医学和外科治疗以及对该疾病生物学的理解方面已经取得了重大进展。然而,基础科学文献往往相互矛盾且令人困惑,缺乏统一的观点。我们报告了BPH分子和细胞基础的当前知识状态。

材料和方法

我们汇编并解释了与BPH发病机制相关的基础科学研究。

结果

包括上皮和基质中增殖、分化、凋亡和衰老变化在内的细胞改变与BPH发病机制有关。分子分析产生了许多在疾病进展中重要的候选基因。BPH组织中细胞因子和生长因子的差异表达提示炎症和缺氧的作用。通过使用细胞培养模型,BPH生长控制的复杂调节机制正在逐渐明确。

结论

科学努力在我们对BPH分子和细胞水平的理解上取得了巨大进展。希望基础科学和转化研究将改善对老年男性这种常见疾病的治疗和预防策略。

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