The mitochondria regulation of stem cell aging

被引:7
|
作者
Wan, Yong [1 ,2 ]
Finkel, Toren [2 ,3 ]
机构
[1] Univ Pittsburgh, Dept Med, Div Endocrinol & Metab, UPMC, Pittsburgh, PA USA
[2] Univ Pittsburgh, Aging Inst, UPMC, Pittsburgh, PA 15219 USA
[3] Univ Pittsburgh, Dept Med, UPMC, Div Cardiol, Pittsburgh, PA USA
关键词
FATTY-ACID OXIDATION; DNA SEQUENCE HETEROGENEITY; SKELETAL-MUSCLE; MUTATIONS ACCUMULATE; AUTOPHAGY MAINTAINS; POINT MUTATIONS; DIFFERENTIATION; PHENOTYPES; DELETIONS; DYNAMICS;
D O I
10.1016/j.mad.2020.111334
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Mitochondrial dysfunction and stem cell exhaustion are among the nine separate hallmarks of aging. Emerging evidence however suggests that mitochondrial activity can have a profound influence on the self-renewal and function of stem cells, thus mechanistically linking mitochondrial function and stem cell decline. In this review, we discuss how accumulation of mtDNA mutations or alterations in mitochondrial dynamics, turnover, and signaling can modulate age-dependent stem cell function. Finally, we also describe how mitochondrial substrate utilization influences stem and progenitor activity. Together, this growing body of evidence suggests that modulation of mitochondrial activity might provide a strategy to slow or reverse age-dependent stem cell decline, and potentially, slow or reverse human aging.
引用
收藏
页数:7
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