Effects of cellular senescence on metabolic pathways in non-immune and immune cells

被引:19
|
作者
Frasca, Daniela [1 ,2 ]
Saada, Yara Bou [3 ]
Garcia, Denisse [1 ]
Friguet, Bertrand [3 ]
机构
[1] Dept Microbiol & Immunol, Miami, FL USA
[2] Univ Miami, Miller Sch Med, Miami, FL 33136 USA
[3] Sorbonne Univ, CNRS, INSERM, Inst Biol Paris Seine,Biol Adaptat & Ageing,B2A I, F-75005 Paris, France
关键词
Cellular senescence; Metabolism; Non-immune cells; Immune cells; HUMAN-FIBROBLASTS; T-CELLS; B-CELLS; REPLICATIVE SENESCENCE; PREMATURE SENESCENCE; INCREASED GLYCOLYSIS; SECRETORY PHENOTYPE; OXIDATIVE STRESS; MEMORY; ACTIVATION;
D O I
10.1016/j.mad.2020.111428
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Many cellular stresses induce cellular senescence and the irreversible arrest of cell proliferation in different cell types. Although blocked in their capacity to divide, senescent cells are metabolically active and are characterized by a different metabolic phenotype as compared to non-senescent cells. Changes observed in senescent cells depend from the cell type and lead to an adaptative flexibility in the type of metabolism. This metabolic reprogramming is needed to cope with survival and with the energetic demands of the senescent program that include the increased secretion of senescence-associated secretory phenotype factors. ABSTRACT Many cellular stresses induce cellular senescence and the irreversible arrest of cell proliferation in different cell types. Although blocked in their capacity to divide, senescent cells are metabolically active and are characterized by a different metabolic phenotype as compared to non-senescent cells. Changes observed in senescent cells depend from the cell type and lead to an adaptative flexibility in the type of metabolism. This metabolic reprogramming is needed to cope with survival and with the energetic demands of the senescent program that include the increased secretion of senescence-associated secretory phenotype factors.
引用
收藏
页数:8
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