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心脏代谢紊乱与勃起功能障碍。

Cardiometabolic Disorder and Erectile Dysfunction.

机构信息

Department of Physiology, Faculty of Basic Medical Sciences, College of Health Sciences, Osun State University, Osogbo, Osun State, Nigeria.

Department of Physiology, Federal University of Technology, Akure, Ondo State, Nigeria.

出版信息

Cell Biochem Biophys. 2024 Sep;82(3):1751-1762. doi: 10.1007/s12013-024-01361-2. Epub 2024 Jun 22.

Abstract

Erectile dysfunction (ED), which is defined as the inability to attain and maintain a satisfactory penile erection to sufficiently permit sexual intercourse, is a consequence and also a cause of cardiometabolic disorders like diabetes mellitus, systemic hypertension, central obesity, and dyslipidemia. Although there are mounting and convincing pieces of evidence in the literature linking ED and cardiometabolic disorders, impairment of nitric oxide-dependent vasodilatation seems to be the primary signaling pathway. Studies have also implicated the suppression of circulating testosterone, increased endothelin-1, and hyperactivation of Ang II/ATIr in the pathogenesis of ED and cardiometabolic disorders. This study provides comprehensive details of the association between cardiometabolic disorders and ED and highlights the mechanisms involved. This would open areas to be explored as therapeutic targets in the management of ED and cardiometabolic disorders. It also provides sufficient evidence establishing the need for the management of cardiometabolic disorders as an adjunct therapy in the management of ED.

摘要

勃起功能障碍(ED)是指无法获得和维持满意的阴茎勃起,从而无法充分进行性交,它是糖尿病、全身性高血压、中心性肥胖和血脂异常等代谢紊乱的结果,也是其病因。尽管文献中有越来越多令人信服的证据表明 ED 与代谢紊乱有关,但一氧化氮依赖的血管舒张功能受损似乎是主要的信号通路。研究还表明,循环睾酮水平降低、内皮素-1 增加和血管紧张素 II/AT1r 过度激活在 ED 和代谢紊乱的发病机制中起作用。本研究全面详细地阐述了代谢紊乱与 ED 之间的关系,并强调了其中涉及的机制。这将为 ED 和代谢紊乱的治疗提供新的靶点,并为 ED 治疗中代谢紊乱的辅助治疗提供充分的证据。

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