衰老
早衰
肿瘤坏死因子α
炎症
生物
TFAM公司
促炎细胞因子
线粒体
细胞生物学
表型
基因剔除小鼠
癌症研究
免疫学
遗传学
基因
线粒体生物发生
作者
Guy Lenaers,Dominique Bonneau,Yves Delneste,Nicolas Papon
标识
DOI:10.1016/j.molmed.2020.07.001
摘要
Desdín-Micó et al. have shown that Tfam specific knockout in mouse T cells disrupts mitochondrial genome integrity and induces a burst of inflammatory cytokines and tumor necrosis factor (TNF)-α production, resulting in increased senescence, neuromuscular and vascular dysfunction, and molecular features that recapitulate premature aging. Interestingly, treatment with nicotinamide riboside (NR) alleviates this phenotype by reducing senescence and systemic inflammation. Desdín-Micó et al. have shown that Tfam specific knockout in mouse T cells disrupts mitochondrial genome integrity and induces a burst of inflammatory cytokines and tumor necrosis factor (TNF)-α production, resulting in increased senescence, neuromuscular and vascular dysfunction, and molecular features that recapitulate premature aging. Interestingly, treatment with nicotinamide riboside (NR) alleviates this phenotype by reducing senescence and systemic inflammation.
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