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Promising molecular targets and biomarkers for male BPH and LUTS.有前途的男性 BPH 和 LUTS 的分子靶点和生物标志物。
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In Utero and Lactational TCDD Exposure Increases Susceptibility to Lower Urinary Tract Dysfunction in Adulthood.子宫内和哺乳期暴露于二噁英会增加成年后患下尿路功能障碍的易感性。
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Lower urinary tract symptoms in men.男性下尿路症状
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Evidence-based treatment strategies in idiopathic pulmonary fibrosis.特发性肺纤维化的循证治疗策略。
Eur Respir Rev. 2013 Jun 1;22(128):163-8. doi: 10.1183/09059180.00001013.
2
Kindlin-2 mediates activation of TGF-β/Smad signaling and renal fibrosis.Kindlin-2 介导 TGF-β/Smad 信号通路的激活和肾脏纤维化。
J Am Soc Nephrol. 2013 Sep;24(9):1387-98. doi: 10.1681/ASN.2012101041. Epub 2013 May 30.
3
The role of chronic prostatic inflammation in the pathogenesis and progression of benign prostatic hyperplasia (BPH).慢性前列腺炎症在良性前列腺增生(BPH)的发病机制和进展中的作用。
BJU Int. 2013 Aug;112(4):432-41. doi: 10.1111/bju.12118. Epub 2013 Apr 12.
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Antifibrotic effects of CXCR4 antagonist in bleomycin-induced pulmonary fibrosis in mice.CXCR4拮抗剂对博来霉素诱导的小鼠肺纤维化的抗纤维化作用。
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5
Obesity-induced diabetes and lower urinary tract fibrosis promote urinary voiding dysfunction in a mouse model.肥胖引起的糖尿病和下尿路纤维化促进小鼠模型的排尿功能障碍。
Prostate. 2013 Jul;73(10):1123-33. doi: 10.1002/pros.22662. Epub 2013 Mar 26.
6
CXC-type chemokines promote myofibroblast phenoconversion and prostatic fibrosis.CXC 型趋化因子促进肌成纤维细胞表型转化和前列腺纤维化。
PLoS One. 2012;7(11):e49278. doi: 10.1371/journal.pone.0049278. Epub 2012 Nov 16.
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Metabolic phenotyping in clinical and surgical environments.临床和手术环境中的代谢表型分析。
Nature. 2012 Nov 15;491(7424):384-92. doi: 10.1038/nature11708.
8
CCL11 (eotaxin-1): a new diagnostic serum marker for prostate cancer.CCL11(趋化因子 11):前列腺癌的新型诊断血清标志物。
Prostate. 2013 May;73(6):573-81. doi: 10.1002/pros.22597. Epub 2012 Oct 11.
9
Prostatic fibrosis is associated with lower urinary tract symptoms.前列腺纤维化与下尿路症状有关。
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Mechanisms of fibrosis: therapeutic translation for fibrotic disease.纤维化机制:纤维化疾病的治疗转化。
Nat Med. 2012 Jul 6;18(7):1028-40. doi: 10.1038/nm.2807.

有前途的男性 BPH 和 LUTS 的分子靶点和生物标志物。

Promising molecular targets and biomarkers for male BPH and LUTS.

机构信息

Center for Personalized Cancer Therapy and the Department of Biology, The University of Massachusetts, Boston, Boston, MA, 02125, USA.

出版信息

Curr Urol Rep. 2013 Dec;14(6):628-37. doi: 10.1007/s11934-013-0368-z.

DOI:10.1007/s11934-013-0368-z
PMID:23913202
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3851290/
Abstract

Benign prostatic hyperplasia (BPH) is a major health concern for aging men. BPH is associated with urinary voiding dysfunction and lower urinary tract symptoms (LUTS), which negatively affects quality of life. Surgical resection and medical approaches have proven effective for improving urinary flow and relieving LUTS but are not effective for all men and can produce adverse effects that require termination of the therapeutic regimen. Thus, there is a need to explore other therapeutic targets to treat BPH/LUTS. Complicating the treatment of BPH/LUTS is the lack of biomarkers to effectively identify pathobiologies contributing to BPH/LUTS or to gauge successful response to therapy. This review will briefly discuss current knowledge and will highlight new studies that illuminate the pathobiologies contributing to BPH/LUTS, potential new therapeutic strategies for successfully treating BPH/LUTS, and new approaches for better defining these pathobiologies and response to therapeutics through the development of biomarkers and phenotyping strategies.

摘要

良性前列腺增生症(BPH)是老年男性的主要健康问题。BPH 与尿流功能障碍和下尿路症状(LUTS)有关,这会降低生活质量。手术切除和药物治疗已被证明可有效改善尿流并缓解 LUTS,但并非对所有男性都有效,并且会产生需要终止治疗方案的不良反应。因此,需要探索其他治疗靶点来治疗 BPH/LUTS。使 BPH/LUTS 的治疗复杂化的是缺乏有效的生物标志物来有效识别导致 BPH/LUTS 的病理生物学,或评估对治疗的成功反应。这篇综述将简要讨论目前的知识,并强调阐明导致 BPH/LUTS 的病理生物学、成功治疗 BPH/LUTS 的潜在新治疗策略,以及通过开发生物标志物和表型策略更好地定义这些病理生物学和对治疗的反应的新方法的新研究。