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糖尿病性勃起功能障碍的病理生理学:神经血管和晚期糖基化终产物的潜在贡献。

Pathophysiology of diabetic erectile dysfunction: potential contribution of vasa nervorum and advanced glycation endproducts.

机构信息

Department of Translational Medicine, Cranfield Health, Cranfield University, Bedfordshire, UK.

出版信息

Int J Impot Res. 2013 Jan;25(1):1-6. doi: 10.1038/ijir.2012.30. Epub 2012 Aug 23.

Abstract

Erectile dysfunction (ED) due to diabetes mellitus remains difficult to treat medically despite advances in pharmacotherapeutic approaches in the field. This unmet need has resulted in a recent re-focus on the pathophysiology, in order to understand the cellular and molecular mechanisms leading to ED in diabetes. Diabetes-induced ED is often resistant to PDE5 inhibitor treatment, thus there is a need to discover targets that may lead to novel approaches for a successful treatment. The aim of this brief review is to update the reader in some of the latest development on that front, with a particular focus on the role of impaired neuronal blood flow and the formation of advanced glycation endproducts.

摘要

尽管在药物治疗领域取得了进展,但由于糖尿病引起的勃起功能障碍(ED)仍然难以治疗。这种未满足的需求导致人们最近重新关注病理生理学,以了解导致糖尿病患者 ED 的细胞和分子机制。糖尿病引起的 ED 通常对 PDE5 抑制剂治疗有抗性,因此需要发现可能为成功治疗提供新方法的靶点。本文简要综述了这方面的最新进展,重点介绍了神经元血流受损和晚期糖基化终产物形成在其中的作用。

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