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睾酮缺乏与血管内皮功能障碍:一氧化氮、非对称性二甲基精氨酸和内皮祖细胞。

Testosterone Deficiency and Endothelial Dysfunction: Nitric Oxide, Asymmetric Dimethylarginine, and Endothelial Progenitor Cells.

机构信息

Department of Hospital Pharmacy, Graduate School of Pharmaceutical Sciences, Nagoya City University, Nagoya, Japan.

Department of Clinical Pharmaceutics, Graduate School of Medical Sciences, Nagoya City University, Nagoya, Japan.

出版信息

Sex Med Rev. 2019 Oct;7(4):661-668. doi: 10.1016/j.sxmr.2019.02.005. Epub 2019 Apr 12.

Abstract

INTRODUCTION

Testosterone deficiency is known to induce endothelial dysfunction, which can lead to erectile dysfunction and/or vascular dysfunction. In some basic and clinical reports, testosterone has been shown to regulate the nitric oxide (NO)/cyclic guanosine monophosphate (cGMP) pathway and thereby influence endothelial function and endothelial progenitor cells (EPCs), which are key for the endothelial repair system.

AIM

To review the association between testosterone and endothelial dysfunction focusing on NO and EPCs.

METHODS

A review of relevant literature up to September 2018 was performed via PubMed.

MAIN OUTCOME MEASURES

We reviewed the association between testosterone and endothelial dysfunction focusing on NO derived from endothelial NO synthase, phosphodiesterase type 5 (PDE-5), asymmetric dimethylarginine (ADMA), inflammation, and EPCs.

RESULTS

Numerous articles describing the association between testosterone deficiency and endothelial dysfunction have been published. Some reports have shown that testosterone deficiency decreases NO production by altering the expression and activity of NO synthase and by regulating ADMA expression. Testosterone also regulates the expression of phosphodiesterase type 5. In addition, some basic and clinical studies have shown that testosterone affects the function and number of EPCs. However, some inconsistencies among these reports have been noted.

CONCLUSION

Testosterone deficiency might cause endothelial dysfunction by decreasing NO levels through regulating the expression and activity of NO synthase and increasing ADMA expression. In addition, testosterone might affect the endothelial repair system by regulating the proliferation and migration of EPCs. Testosterone replacement therapy might be useful for treating endothelial dysfunction, considering that some reports have shown that this therapy improved NO bioavailability and EPC function. Hotta Y, Kataoka T, Kimura K. Testosterone Deficiency and Endothelial Dysfunction: Nitric Oxide, Asymmetric Dimethylarginine, and Endothelial Progenitor Cells. Sex Med Rev 2019;7:661-668.

摘要

简介

已知睾丸激素缺乏会导致内皮功能障碍,从而导致勃起功能障碍和/或血管功能障碍。在一些基础和临床报告中,已经表明睾丸激素可以调节一氧化氮(NO)/环磷酸鸟苷(cGMP)途径,从而影响内皮功能和内皮祖细胞(EPC),这对于内皮修复系统至关重要。

目的

综述睾丸激素与内皮功能障碍之间的关系,重点关注一氧化氮和内皮祖细胞。

方法

通过 PubMed 对截至 2018 年 9 月的相关文献进行了回顾。

主要观察指标

我们综述了睾丸激素与内皮功能障碍之间的关系,重点关注来自内皮型一氧化氮合酶、磷酸二酯酶 5(PDE-5)、不对称二甲基精氨酸(ADMA)、炎症和内皮祖细胞的一氧化氮。

结果

已经发表了许多描述睾丸激素缺乏与内皮功能障碍之间关系的文章。一些报告表明,睾丸激素缺乏通过改变一氧化氮合酶的表达和活性以及调节 ADMA 表达来减少一氧化氮的产生。睾丸激素还调节磷酸二酯酶 5 的表达。此外,一些基础和临床研究表明,睾丸激素影响内皮祖细胞的功能和数量。然而,这些报告之间存在一些不一致之处。

结论

睾丸激素缺乏可能通过调节一氧化氮合酶的表达和活性以及增加 ADMA 表达来降低一氧化氮水平,从而导致内皮功能障碍。此外,睾丸激素可能通过调节内皮祖细胞的增殖和迁移来影响内皮修复系统。考虑到一些报告表明这种治疗方法提高了一氧化氮的生物利用度和内皮祖细胞的功能,睾丸激素替代疗法可能对治疗内皮功能障碍有用。Hotta Y, Kataoka T, Kimura K. 睾丸激素缺乏与内皮功能障碍:一氧化氮、不对称二甲基精氨酸和内皮祖细胞。性医学评论 2019;7:661-668。

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