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糖尿病性勃起功能障碍与阴茎海绵体平滑肌细胞表型转化的相关研究进展     被引量:1

A review on the correlation between diabetic erectile dysfunction and phenotypic transformation of corporal cavernous smooth muscle cell

文献类型:期刊文献

中文题名:糖尿病性勃起功能障碍与阴茎海绵体平滑肌细胞表型转化的相关研究进展

英文题名:A review on the correlation between diabetic erectile dysfunction and phenotypic transformation of corporal cavernous smooth muscle cell

作者:冀小卫[1];刘黎明[1];张爱平[1];邢喜平[2];王新平[2]

第一作者:冀小卫

机构:[1]甘肃中医药大学中西医结合学院,甘肃兰州730000;[2]甘肃中医药大学附属医院,甘肃兰州730020

第一机构:甘肃中医药大学中西医结合学院

年份:2023

卷号:15

期号:31

起止页码:34

中文期刊名:中医临床研究

外文期刊名:Clinical Journal Of Chinese Medicine

基金:2021年甘肃省重点人才项目(中医男科人才团队建设及男性性功能障碍中医诊疗技术推广应用);甘肃省中医药防治慢性病重点实验室开放基金(GSMBKY2015-13)。

语种:中文

中文关键词:糖尿病性勃起功能障碍;阴茎海绵体平滑肌细胞;表型转化;标志性蛋白;综述

外文关键词:Diabetic erectile dysfunction;Penile cavernous smooth muscle cells;Phenotypic transformation;Landmark protein;Review

摘要:糖尿病性勃起功能障碍(Diabetic Erectile Dysfunction,DMED)与阴茎海绵体平滑肌细胞(Corporal Cavernous Smooth Muscle Cells,CCSMC)表型转化关系密切。CCSMC表型转化是一种CCSMC由“收缩型”向“合成型”或“增殖型”转化的趋势。阴茎的勃起是神经-内分泌调节下的海绵体血流动力学变化过程,其中CCSMC的舒张在此过程中起着关键作用。CCSMC表型转化的标志性蛋白包括收缩型和合成型,前者包括α-平滑肌肌动蛋白(α-Smooth Muscle Actin,α-SMA)、平滑肌肌球蛋白重链(Smooth Muscle Myosin Heavy Chain,SMMHC)等;后者包括骨桥蛋白(Osteopontin,OPN)、波形蛋白等蛋白。若收缩型蛋白表达下调或合成型蛋白表达上调,则提示CCSMC发生表型转化,反之称为逆表型转化。研究表明,DMED大鼠CCSMC中α-SMA等收缩型标志物表达下降,而OPN等合成型(增殖型)标志物上升,显示DMED可以促使CCSMC发生表型转化。DMED的发病机制包括血管病变、神经病变、阴茎海绵体平滑肌因素、神经递质调节、内分泌紊乱等因素。当前,大多数学者皆从血管病变方面研究DMED与CCSMC表型转化之间的关系。研究表明,CCSMC表型转化会导致阴茎海绵体结构发生改变,进而影响DMED患者的勃起功能。文章根据目前研究成果,对DMED与CCSMC表型转化相关研究进行系统回顾,以期寻求一种治疗DMED的新思路,从而更好地造福人类。
Diabetic erectile dysfunction(DMED)is closely related to phenotypic transformation of corporal cavernous smooth muscle cells(CCSMC).CCSMC phenotypic transformation is a trend of CCSMC transformation from contractile to synthetic or proliferative.Penile erection is a process of cavernous hemodynamic changes regulated by neuroendocrine,in which the relaxation of CCSMC plays a key role.The signature proteins of CCSMC phenotypic transformation include contractile protein and synthetic protein,and the former includesα-smooth muscle actin(α-SMA),smooth muscle myosin heavy chain(SMMHC),etc..The latter includes osteopontin(OPN),vimentin and so on.If contractile protein expression is down-regulated or synthetic protein expression is upregulated,it indicates that the phenotypic transformation occurs in CCSMC,otherwise,it is called reverse phenotypic transformation.The studies show that the expressions of contractile markers such asα-SMA were decreased in CCSMC of DMED rats,while the expressions of proliferative markers such as OPN were increased,indicating that DMED could promote the phenotypic transformation of CCSMC.The pathogenesis of DMED includes vascular disease,neuropathy,smooth muscle factors of penile cavernosa,neurotransmitter regulation,endocrine disorders and other factors.At present,most scholars have studied the relationship between DMED and phenotypic transformation of CCSMC from the aspect of vascular disease.Studies have shown that the phenotypic transformation of CCSMC can lead to structural changes in the cavernous body of the penis,thus affecting erectile function of DMED patients.Based on the current research results,a systematic review of the studies on the correlation between DMED and phenotypic transformation of CCSMC is conducted in this paper to seek a new idea for the treatment of DMED,so as to better benefit mankind.

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