Penile erectile dysfunction (ED) is ascribed to the contraction-relaxation imbalance of smooth muscle cells (SMC), the weakening of their diastolic function and the strengthening of their systolic function. The contraction-related signaling pathways, cell membrane ion channels and SMC phenotypes all participate in the regulation of their contraction and its malfunction may cause a variety of SMC-related diseases. The signaling pathways RhoA/Rock and Raf/MEK/ERK1/2 interact with each other, suppressing the expression of the RhoA protein or reducing the level of Rock2 phosphorylation, which may contribute to the treatment of ED. The poor performance of VDCC or TRPC is reckoned to be an important cause of hypertension- or diabetes-related ED. The expressions of CaV1.2, TRPC1 and TRPC4 can be upregulated by many pathological factors, which may enhance the contraction of SMCs. The pathogenesis of ED may be associated with the differentiation of the phenotypes corpus cavernosal SMCs. This review focuses on the recent progress in the studies of the relationship between SMC contraction and ED.
阴茎勃起功能障碍(ED)与平滑肌细胞的收缩与舒张失衡相关。ED发生过程中，除舒张功能减弱外，另一重要原因为平滑肌细胞的收缩功能上调。其中，收缩相关性信号通路、胞膜离子通道、平滑肌细胞表型都参与了平滑肌细胞收缩的调节，其功能变化可引起多种平滑肌细胞相关疾病。收缩相关性信号通路Raf/MEK/ERK1/2与RhoA/Rock 通路之间存在交互作用，抑制RhoA蛋白表达或降低Rock2磷酸化水平都可能成为ED的治疗途径。电压依赖性钙通道(VDCCs)、瞬时受体电位(TRP)通道功能失调是高血压、糖尿病ED发病的主要原因之一，多种病理因素上调CaV1.2、TRPC1及TRPC4表达可使平滑肌收缩功能加强，进而导致ED的发生；阴茎海绵体表型转化也与ED的发生发展有关。本文就近年平滑肌收缩机制与ED关系研究的进展加以综述。.
Keywords: contraction; smooth muscle cell; erectile dysfunction.