蛋白质组学

糖尿病相关勃起障碍治疗分子靶标筛选

勃起功能障碍是男性最常见的糖尿病引起的并发症之一,目前评估表明,多达75%的男性糖尿病患者会有一定程度的勃起功能障碍,而且在许多病例中糖尿病患者会有更严重的勃起功能障碍,对常用勃起药物反应较差。

细胞分析蛋白组学三月份有篇研究报道,来自凯斯西储大学和阿尔伯特爱因斯坦医学院的研究人员证实随着糖尿病诱发ED的发生,出现了分子的改变,这可以作为帮助确认ED风险的标记以及作为潜在的药物靶点。

Mark Chance和他的同事们应用蛋白组学方法检测糖尿病大鼠两个不同发展阶段体内蛋白质的相对量(勃起时充血阴茎增大的组织):患糖尿病后的一周和两个月。将这些大鼠与作为对照的相同年龄的健康大鼠进行比较,确定糖尿病大鼠的阴茎组织中有57种蛋白质增高或降低。

选择的蛋白揭示了ED的机理,不出所料的是,糖尿病患者的胶原蛋白(给组织提供强度和硬度)以及运输性激素的蛋白也许会下调。同时,包含在凋亡细胞中的蛋白质上调,同样还有许多与脂肪新陈代谢有关的蛋白质,这些改变可能与血管的缩小和硬化有关。

Mark Chance和他的同事们指出,他们研究所用的动物模型模拟了很多人类勃起功能障碍相关的特征,因此,鉴定这57种候选蛋白可以对人类糖尿病和勃起功能障碍之间的关系做进一步的阐释以及更详细的研究,并获得对疾病的诊断和研究出药物靶点。

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Identifying Molecular Targets for Diabetes-Related Erectile Dysfunction


Erectile dysfunction is one of the most prevalent diabetes-induced complications in men; current estimates suggest that as many as 75% of men with diabetes will develop some degree of erectile dysfunction, and in many cases diabetics develop more severe forms of ED that are less responsive to standard drugs.

Now, in a study appearing in the March Molecular and Cellular Proteomics, researchers at Case Western Reserve University and Albert Einstein College of Medicine have identified some of the molecular changes that accompany the onset of diabetes-induced ED, which may lead to markers that will help identify ED risk as well as new potential drug targets.

Mark Chance and colleagues used a proteomics approach to examine the relative abundance of proteins in the corpora (the expandable tissues along the length of the penis which fill with blood during erection) of diabetic rats at two different stages of progression: one week and two months after the onset of diabetes. By comparing these rats to healthy age-matched controls, they identified 57 proteins in the penile tissue that either increased or decreased during diabetes.

The candidate proteins revealed insights into the mechanics of ED; perhaps not surprisingly, collagen proteins that provide strength and stiffness were down-regulated in diabetes, as were proteins that transport sex hormones. Meanwhile, proteins involved in cell death (apoptosis) were up-regulated, as were many proteins related to fat metabolism, changes that might be related to narrowing or hardening of blood vessels.

Chance and colleagues note that the rat model they used in the study mimics many relevant features of human ED, and thus the identification of these 57 candidate proteins could open up further and more detailed studies into the relationship between diabetes and ED in humans, and also lead to diagnostic and drug targets.

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