[Peptide regulation of cellular aging.]

O M Ivko
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引用次数: 0

Abstract

Cellular aging is the inability of structures to proliferate (further division) and repair damage while maintaining metabolic activity. The key well-known factors of cellular aging are the processes of DNA damage, telomere shortening, the development of oxidative stress and epigenetic changes. The above factors provoke the development of a pro-inflammatory environment, leading to errors in gene expression and metabolic dysregulation, thereby affecting the development of age-related diseases that contribute to pathological changes in the functions of tissues and organs. Modern pharmacotherapy approaches aimed at slowing down the processes of cellular aging are mainly focused on three key strategies: influencing the signaling pathways that cause cellular aging, as well as specific factors of the cell cycle (protein structures - receptors, carrier proteins, bioregulators, and so on), improving the elimination of cellular debris by the immune systern pharmacotherapy approaches aimed at slowing down the processes of cellular aging are mainly focused on three key strategies: influencing the signaling pathways that cause cellular aging, as well as specific factors of the cell cycle (protein structures - receptors, carrier proteins, bioregulators, and so on), improving the elimination of cellular debris by the immune system. In the elderly, the regulation of various processes of the cell cycle is disrupted, and the use of polypeptide complexes helps to maintain normal body functions by stimulating the synthesis of proteins-markers of cell functional activity.

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[细胞衰老的肽调节。]
细胞老化是指结构在维持代谢活动的同时无法增殖(进一步分裂)和修复损伤。众所周知,细胞衰老的关键因素是DNA损伤、端粒缩短、氧化应激和表观遗传变化的过程。上述因素引发促炎环境的发展,导致基因表达错误和代谢失调,从而影响年龄相关疾病的发展,导致组织和器官功能的病理改变。旨在减缓细胞衰老过程的现代药物治疗方法主要集中在三个关键策略上:影响导致细胞衰老的信号通路,以及细胞周期的特定因素(蛋白质结构-受体、载体蛋白、生物调节剂等),通过免疫系统药物治疗方法改善细胞碎片的消除,旨在减缓细胞衰老过程,主要集中在三个关键策略上:影响导致细胞衰老的信号通路,以及细胞周期的特定因素(蛋白质结构-受体,载体蛋白,生物调节剂等),改善免疫系统对细胞碎片的清除。在老年人中,细胞周期的各种过程的调节被打乱,多肽复合物的使用通过刺激蛋白质的合成来帮助维持正常的身体功能,蛋白质是细胞功能活性的标志。
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来源期刊
CiteScore
0.50
自引率
0.00%
发文量
131
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