Posttranslational modification of constitutive nitric oxide synthase in the penis.
Posttranslational modification of constitutive nitric oxide synthase in the penis.
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DOI：
10.2164/jandrol.108.006999
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发表时间：
2009-07
影响因子：
--
通讯作者：
Bivalacqua TJ
中科院分区：
文献类型：
--
作者：
Musicki B;Ross AE;Champion HC;Burnett AL;Bivalacqua TJ
勃起功能障碍 (ED) 是一种常见的男性健康问题，其特征是始终无法维持足以进行性交的勃起。勃起生理学的基础科学研究一直致力于研究 ED 的发病机制，并得出这样的结论：ED 主要是一种血管起源和/或神经源性功能障碍的疾病。一氧化氮合酶[NOS；内皮型一氧化氮合酶（eNOS）和神经型一氧化氮合酶（nNOS）]是参与一氧化氮（NO）产生的重要酶，从而调节阴茎血管稳态。鉴于内皮和神经元来源的一氧化氮在阴茎血管生物学中的影响，过去十年的大量研究都集中在内皮和氮能神经末梢合成一氧化氮在正常勃起生理和疾病状态中的作用。内皮功能完整性的丧失和随后的内皮功能障碍在 ED 的发生中起着不可或缺的作用。因此，ED 发展过程中涉及这些 NOS 亚型失调的分子机制对于发现各种疾病状态下 ED 的发病机制至关重要。本次通讯回顾了 eNOS 和 nNOS 在勃起生理学中的作用，并讨论了阴茎各种血管疾病中 eNOS 和 nNOS 通过翻译后修饰而发生的改变。
Erectile dysfunction (ED) is a common men's health problem characterized by the consistent inability to sustain an erection sufficient for sexual intercourse. Basic science research on erectile physiology has been devoted to investigating the pathogenesis of ED and has led to the conclusion that ED is predominately a disease of vascular origin and/or neurogenic dysfunction. The constitutive forms of nitric oxide synthase [NOS; endothelial NOS (eNOS) and neuronal NOS (nNOS)] are important enzymes involved in the production of nitric oxide (NO) and thus regulate penile vascular homeostasis. Given the impact of endothelial- and neuronal-derived NO in penile vascular biology, a great deal of research over the past decade has focused on the role of NO synthesis from the endothelium and nitrergic nerve terminal in normal erectile physiology as well as in disease states. Loss of the functional integrity of the endothelium and subsequent endothelial dysfunction plays an integral role in the occurrence of ED. Therefore, molecular mechanisms involved in dysregulation of these NOS isoforms in the development of ED are essential to discovering the pathogenesis of ED in various disease states. This communication reviews the role of eNOS and nNOS in erectile physiology and discusses the alterations in eNOS and nNOS via post-translation modification in various vascular diseases of the penis.
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