Mechanisms of Penile Fibrosis
Mechanisms of Penile Fibrosis
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DOI：
10.1111/j.1743-6109.2008.01195.x
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发表时间：
2009-03-01
影响因子：
3.5
通讯作者：
Gonzalez-Cadavid, Nestor F.
中科院分区：
文献类型：
--
作者：
Gonzalez-Cadavid, Nestor F.
导言。阴茎纤维化在概念上被认为是在阴茎膜上形成的斑块：Peyronie病(PD)中的白膜，或者是由缺血或创伤事件引起的海绵体局部突起。最近，有人提出，弥漫性、进行性和弥漫性的临床区纤维化，也影响到阴茎动脉的中层，是与年龄、吸烟、糖尿病、高血压和前列腺癌根治术后相关的血管性勃起功能障碍(ED)有关的原因。这些过程在病因、染色过程、靶细胞和治疗方法上有所不同，但有许多共同的特点。回顾有关阴茎纤维化的文献，与帕金森病和勃起功能障碍相关。PubMed主要检索2001-2008年间的相关文献。本文首先对帕金森病进行了综述，然后介绍了在动物细胞培养模型中对ED的研究，讨论了PD间质纤维化与小体静脉闭塞功能障碍(CVOD)之间的病理生理学相似性，以及新出现的治疗策略。促纤维因子的作用，胶原纤维和其他细胞外基质的过度沉积，合成细胞表型的出现或成纤维细胞-肌成纤维细胞转变的开始，以及在阴茎动脉或体动脉组织中，平滑肌细胞间隔的减少，都被讨论过。这种组织病理学导致阴茎组织的局限性斑块或结节，或导致弥漫性纤维化，导致组织顺应性受损，这是CVOD和动脉性ED的基础。还简要介绍了阴茎持续刺激一氧化氮/环鸟苷一磷酸途径的抗纤维化作用及其可能与外源性ALLOT内源性Stein细胞分化的关系。阴茎组织中的纤维化过程具有相似的细胞和分子病理生理学以及共同的内源性防御机制，这些都激发了新的药理学实验方法。Gonzalez-Cadavid NF：阴茎纤维化的机制。《性医学杂志》2009；6(增刊3)：353-362。
Introduction. Penile fibrosis has been conceptually identified with the plaque that develops in the tunica :albuginea in Peyronie's disease (PD), or with localized processes induced in the corpora cavernosa by ischemic or traumatic events. Recently, it has been proposed that a diffuse, progressive, and guilder intracorporal fibrosis, which affects also the media of the penile arteries, is responsible for vasculogenic erectile dysfunction (ED) associated with aging, smoking, diabetes, hypertension, and post-radical prostatectomy. These processes differ in etiology, tinge course, target cells, and treatment, but have many features in common.Aim. To review the literature pertaining to fibrosis in the penis, related to PD and ED.Methods. PubMed search for pertinent publications mainly during 2001-2008.Results. This review focuses initially on PD and then deals with studies on ED in animal cell culture models, discussing sonic of the pathophysiological similarities between tunical fibrosis ill PD mid corporal fibrosis ill corporal veno-occlusive dysfunction (CVOD), and emerging therapeutic strategies. The role of profibrotic factors, the excessive deposit of collagen fibers and other extracellular matrix, the appearance of a synthetic cell phenotype ill smooth muscle cells or the onset of a fibroblast-myofibroblast transition, and in the case of the corporal or penile arterial tissue the reduction of the smooth muscle cellular compartment, are discussed. This histopathology leads either to localized plaques or nodules ill penile tissues, or to the diffuse fibrosis causing impairment of tissue compliance that underlies CVOD and arteriogenic ED. The antifibrotic role of the sustained stimulation of the nitric oxde/cyclic guanosine monophosphate pathway in the penis and its possible relevance to exogenous allot endogenous stein cell differentiation is also briefly presented.Conclusions. Fibrotic processes in penile tissues share a similar cellular and molecular pathophysiology and common endogenous mechanisms of defense that have inspired novel pharmacological experimental approches. Gonzalez-Cadavid NF: Mechanisms of penile fibrosis. J Sex Med 2009;6(suppl 3):353-362.