Laboratory of Experimental Urology, University Hospitals Leuven, Leuven, Belgium.
J Sex Med. 2012 Feb;9(2):385-403. doi: 10.1111/j.1743-6109.2011.02556.x. Epub 2011 Dec 6.
Erectile dysfunction (ED) following radical prostatectomy (RP) is a result of inadvertent damage to the cavernous nerves that run close to the prostate capsula. The mechanisms behind the development of post-RP ED are increasingly recognized and include cavernosal fibrosis and cavernosal smooth muscle apoptosis, resulting from cavernous nerve degeneration due to neuropraxia. In recent years, cell-based therapies have received increasing attention regarding their potential for recovery of erectile function following cavernous nerve injury (CNI). Multipotent stromal cells (MSCs) are an attractive cell source for this application based on their regenerative potential and their clinical applicability.
To review available evidence on the efficacy and mechanisms of action of MSC application for the treatment of ED, with an emphasis on ED following CNI.
A nonsystematic review was conducted on the available English literature between 1966 and 2011 on the search engines SciVerse-sciencedirect, SciVerse-scopus, Google Scholar, and PubMed.
MSCs from both bone marrow and adipose tissue have shown beneficial effects in a variety of animal models for ED. While MSC application in chronic disease models such as diabetes, aging, and hyperlipidemia may result in cell engraftment and possibly MSC differentiation, this observation has not been made in the acute CNI rat model. In the latter setting, MSC effects seem to be established by cell recruitment toward the major pelvic ganglion and local paracrine interaction with the host neural tissue.
While the type of model may influence the mechanisms of action of this MSC-based therapy, MSCs generally display efficacy in various animal models for ED. Before translation to the clinic is established, various hurdles need to be overcome.
根治性前列腺切除术（RP）后发生的勃起功能障碍（ED）是由于靠近前列腺包膜的海绵体神经意外损伤所致。导致 RP 后 ED 的机制越来越被认识，包括海绵体纤维化和海绵体平滑肌凋亡，这是由于海绵体神经由于神经损伤而退化导致的。近年来，细胞疗法因其在海绵体神经损伤（CNI）后恢复勃起功能的潜力而受到越来越多的关注。多能基质细胞（MSCs）因其再生潜能和临床适用性，成为这种应用的有吸引力的细胞来源。
综述目前关于 MSC 应用治疗 ED 的疗效和作用机制的证据，重点关注 CNI 后 ED。
在 1966 年至 2011 年期间，在 SciVerse-sciencedirect、SciVerse-scopus、Google Scholar 和 PubMed 搜索引擎上进行了非系统性综述，检索了英文文献。
来自骨髓和脂肪组织的 MSC 在多种 ED 动物模型中均显示出有益作用。虽然 MSC 应用于糖尿病、衰老和高脂血症等慢性疾病模型可能导致细胞移植和 MSC 分化，但在急性 CNI 大鼠模型中尚未观察到这种情况。在后一种情况下，MSC 的作用似乎是通过细胞向主骨盆神经的募集和与宿主神经组织的局部旁分泌相互作用来建立的。
虽然模型的类型可能会影响这种基于 MSC 的治疗的作用机制，但 MSC 通常在各种 ED 动物模型中显示出疗效。在将其转化为临床应用之前，需要克服各种障碍。
