气候变化领域集成服务门户(CCPortal): T cells with dysfunctional mitochondria induce multimorbidity and premature senescence

CCPortal

DOI	10.1126/science.aax0860
	T cells with dysfunctional mitochondria induce multimorbidity and premature senescence
	Desdín-Micó G.; Soto-Heredero G.; Aranda J.F.; Oller J.; Carrasco E.; Gabandé-Rodríguez E.; Blanco E.M.; Alfranca A.; Cussó L.; Desco M.; Ibañez B.; Gortazar A.R.; Fernández-Marcos P.; Navarro M.N.; Hernaez B.; Alcamí A.; Baixauli F.; Mittelbrunn M.
发表日期	2020
ISSN	0036-8075
起始页码	1371
结束页码	1376
卷号	368 期号:6497
英文摘要	The effect of immunometabolism on age-associated diseases remains uncertain. In this work, we show that T cells with dysfunctional mitochondria owing to mitochondrial transcription factor A (TFAM) deficiency act as accelerators of senescence. In mice, these cells instigate multiple aging-related features, including metabolic, cognitive, physical, and cardiovascular alterations, which together result in premature death. T cell metabolic failure induces the accumulation of circulating cytokines, which resembles the chronic inflammation that is characteristic of aging (“inflammaging”). This cytokine storm itself acts as a systemic inducer of senescence. Blocking tumor necrosis factor-a signaling or preventing senescence with nicotinamide adenine dinucleotide precursors partially rescues premature aging in mice with Tfam-deficient T cells. Thus, T cells can regulate organismal fitness and life span, which highlights the importance of tight immunometabolic control in both aging and the onset of age-associated diseases. © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works
关键词	cardiovascular disease enzyme activity gene expression metabolism mitochondrial DNA morbidity senescence tumor Mus DNA binding protein mitochondrial protein mitochondrial transcription factor A nicotinamide adenine dinucleotide transcription factor tumor necrosis factor animal cytokine release syndrome female fitness gene deletion genetics immunology inflammation longevity male metabolism mitochondrion mouse multiple chronic conditions mutant mouse strain premature aging T lymphocyte ultrastructure Aging, Premature Animals Cytokine Release Syndrome DNA-Binding Proteins Female Gene Deletion Inflammation Longevity Male Mice Mice, Mutant Strains Mitochondria Mitochondrial Proteins Multimorbidity NAD Physical Fitness T-Lymphocytes Transcription Factors Tumor Necrosis Factor-alpha
语种	英语
来源机构	Science
文献类型	期刊论文
条目标识符	http://gcip.llas.ac.cn/handle/2XKMVOVA/133423
推荐引用方式 GB/T 7714	Desdín-Micó G.,Soto-Heredero G.,Aranda J.F.,et al. T cells with dysfunctional mitochondria induce multimorbidity and premature senescence[J]. Science,2020,368(6497).
APA	Desdín-Micó G..,Soto-Heredero G..,Aranda J.F..,Oller J..,Carrasco E..,...&Mittelbrunn M..(2020).T cells with dysfunctional mitochondria induce multimorbidity and premature senescence.,368(6497).
MLA	Desdín-Micó G.,et al."T cells with dysfunctional mitochondria induce multimorbidity and premature senescence".368.6497(2020).