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Targeting Endothelin in Alzheimer’s Disease: A Promising Therapeutic Approach
BioMed Research International ( IF 3.246 ) Pub Date : 2021-09-07 , DOI: 10.1155/2021/7396580
Shiwali Sharma 1 , Tapan Behl 1 , Anoop Kumar 2 , Aayush Sehgal 1 , Sukhbir Singh 1 , Neelam Sharma 1 , Saurabh Bhatia 3, 4 , Ahmed Al-Harrasi 3 , Simona Bungau 5
Affiliation  

Endothelin is a chemical mediator that helps in maintaining balance within the blood-brain barrier by regulating the levels of toxicants and molecules which pass through the brain, suggesting that a rise in its production determines Alzheimer’s disease. The inequity in the amyloid β occurs due to a problem in its clearance from the brain initiating the production of reactive oxygen species and superoxide that activates a cascade wherein the release of inflammatory mediators and various enzymes like endothelin-converting enzymes take place. Furthermore, the cascade increases the levels of endothelin in the brain from endothelial cells. Endothelin levels are upregulated, which can be regulated by modulating the action of endothelin-converting enzymes and endothelin receptors. Hence, endothelin paves a pathway in the treatment of Alzheimer’s disease. In this article, we have covered various mechanisms and preclinical studies that support and direct endothelin involvement in the progression of Alzheimer’s disease by using various search tools such as PubMed, Science Direct, and Medline. Conclusive outcome data were extracted that all together defy contrivance pathways, potential drugs, endothelin receptors, and endothelin enzymes in our article giving profound importance to target endothelin for prevention and treatment of Alzheimer’s disease.

中文翻译:

在阿尔茨海默病中靶向内皮素:一种有前景的治疗方法

内皮素是一种化学介质,通过调节通过大脑的毒物和分子的水平来帮助维持血脑屏障内的平衡,这表明其产生的增加决定了阿尔茨海默病。β淀粉样蛋白的不公平性由于其从大脑中清除的问题,引发了活性氧和超氧化物的产生,从而激活了级联反应,其中发生了炎症介质和各种酶(如内皮素转化酶)的释放。此外,级联反应增加了大脑内皮细胞内皮素的水平。内皮素水平被上调,这可以通过调节内皮素转化酶和内皮素受体的作用来调节。因此,内皮素为阿尔茨海默病的治疗铺平了道路。在本文中,我们通过使用 PubMed、Science Direct 和 Medline 等各种搜索工具,介绍了支持和指导内皮素参与阿尔茨海默病进展的各种机制和临床前研究。
更新日期:2021-09-07
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