抑制促炎因子TNF/Edn1通路对衰老细胞重编程的细胞衰老研究

Siwen Cui, Virgia Wang
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引用次数: 0

摘要

衰老是细胞衰老和组织退化的过程,最终导致机体死亡。这种退化表现为各种与年龄有关的疾病,如神经退行性疾病、糖尿病和慢性炎症。虽然最初被认为是人类生命不可避免的最终命运,但越来越多的证据表明,它有延长寿命和减缓衰老过程的可能性。从这些观察结果来看,是否可以通过细胞再生来逆转衰老的问题激发了进一步的研究。在人类中,生殖细胞在受精事件中激活了一个自然的返老还童程序,这表明细胞年龄逆转的可能性。虽然潜在机制的细微差别尚不清楚,但衰老过程中表观基因组的重编程似乎起着核心作用。该项目旨在通过直接比较衰老细胞和年轻细胞(与来自人骨髓来源的基质细胞、小鼠视网膜神经节细胞和小鼠成纤维细胞的基因表达数据),确定候选年龄重编程基因作为OSKM的替代品。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Research on Cell Aging Based on Reprogramming Senescent Cells by Inhibiting Pro-Inflammatory TNF/Edn1 Pathway as a Potential Treatment of Age-Related Diseases
Aging is the process of progressive cellular senescence and tissue degeneration that eventually leads to organismal death. This degeneration manifests itself in the forms of various age-related diseases, such as neurodegenerative disorders, diabetes, and chronic inflammation. Although initially believed to be the inevitable final fate of human life, mounting evidence demonstrate the possibility to extend lifespan and decelerate the process of aging. From these observations, the question of whether aging can be reversed through cellular rejuvenation inspires further research. In humans, germline cells activate a natural program of rejuvenation in fertilization events, suggesting the possibility of cellular age reversal. While the nuance of the underlying mechanism is unclear, reprogramming the epigenome during aging seems to play central role.This project aims to identify candidate age reprogramming genes as alternatives to OSKM through directly comparing senescent and young cells (with gene expression data from human bone marrow-derived stromal cells, mouse retinal ganglion cells, and mouse fibroblasts).
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