规范与病理中的小窝行为

Basheer Abdullah Marzoog
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引用次数: 0

摘要

小窝蛋白是一种普遍存在的多功能生理活性微粒,在小窝形成过程中协同作用,维持细胞的代谢稳态平衡。事实上,近年来,通过探索小窝在正常和生理病理中的作用,小窝的分子生物病理学取得了显着的进展。对目前关于小窝行为规范和病理的文献资料进行了修订。小囊泡在各种细胞类型中表达,高度集中在内皮细胞、心肌细胞和上皮细胞中。生理上,通过调节酪氨酸激酶、G蛋白偶联受体、内皮型一氧化氮合酶、糖原合酶激酶3β、p42/p44丝裂原活化蛋白激酶、PKA、SFK、PKC、Akt通路,小囊泡有助于维持各种稳态过程之间的信号平衡,包括促生长和促生存过程。它们的信号功能障碍与心血管疾病、再生抑制、神经退行性疾病、感染、骨质疏松、糖尿病和肿瘤诱导和进展的发病机制直接相关。调节小泡活性/表达的比例和外显率是一种具有临床意义的潜在治疗策略,可以增强当前的治疗方法,消除不断上升的体内平衡疾病的发病途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Caveolae’s Behavior in Norm and Pathology
Caveolins are universal multifunctional physiologically active microparticles that collaborate in the caveolae formation to maintain the metabolic homeostatic balance of the cells. In fact, remarkable advances in the molecular biopathology of caveolae have been made in recent years by exploring the role of caveolae in norm and physiopathology. The current literature data on the caveolae behavior in norm and pathology were revised. Caveolae are expressed in various cell types, highly concentrated in endothelial cells, cardiomyocytes, and epithelial cells. Physiologically, caveolae contribute to maintaining a signaling balance between the various homeostatic processes, including pro-growth and pro-survival, such as endothelial nitric oxide synthase, glycogen synthase kinase-3β, p42/p44 mitogen-activated protein kinase, PKA, SFK, PKC, Akt through regulation of tyrosine kinases, G protein-coupled receptor, endothelial nitric oxide synthase, and MAPK pathways, and their signaling dysfunction is directly attributed to the pathogenesis of cardiovascular diseases, regeneration inhibition, neurodegenerative diseases, infection, osteoporosis, diabetes, and tumour induction and progression. Regulation of the ratio and penetrance of caveolae activity/expression is a clinically significant potential therapeutic strategy to enhance the current therapies and eliminate the etiopathogenetic pathway of rising homeostatic disorders.
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