Aging: All roads lead to mitochondria.
Aging: All roads lead to mitochondria.
复制标题
DOI:
10.1016/j.semcdb.2021.02.006
复制
发表时间:
2021-08
影响因子:
7.3
通讯作者:
Lee, Changhan
中科院分区:
文献类型:
--
作者:
Son, Jyung Mean;Lee, Changhan
Mitochondria were described as early as 1890 as ubiquitous intracellular structures by Ernster and Schatz (1981). Since then, the accretion of knowledge in the past century has revealed much of the molecular details of mitochondria, ranging from mitochondrial origin, structure, metabolism, genetics, and signaling, and their implications in health and disease. We now know that mitochondria are remarkably multifunctional and deeply intertwined with many vital cellular processes. They are quasi-self organelles that still possess remnants of its bacterial ancestry, including an independent genome. The mitochondrial free radical theory of aging (MFRTA), which postulated that aging is a product of oxidative damage to mitochondrial DNA, provided a conceptual framework that put mitochondria on the map of aging research. However, several studies have more recently challenged the general validity of the theory, favoring novel ideas based on emerging evidence to understand how mitochondria contribute to aging and age-related diseases. One prominent topic of investigation lies on the fact that mitochondria are not only production sites for bioenergetics and macromolecules, but also regulatory hubs that communicate and coordinate many vital physiological processes at the cellular and organismal level. The bi-directional communication and coordination between the co-evolved mitochondrial and nuclear genomes is especially interesting in terms of cellular regulation. Mitochondria are dynamic and adaptive, rendering their function sensitive to cellular context. Tissues with high energy demands, such as the brain, seem to be uniquely affected by age-dependent mitochondrial dysfunction, providing a foundation for the development of novel mitochondrial-based therapeutics and diagnostics.
登录
查看更多内容
影响因子:
4.5
作者:
Ameur A;Stewart JB;Freyer C;Hagström E;Ingman M;Larsson NG;Gyllensten U
通讯作者:
Gyllensten U
影响因子:
64.5
作者:
Chen H;Vermulst M;Wang YE;Chomyn A;Prolla TA;McCaffery JM;Chan DC
通讯作者:
Chan DC
影响因子:
11.4
作者:
Area-Gomez, Estela;Castillo, Maria Del Carmen Lara;Tambini, Marc D.;Guardia-Laguarta, Cristina;de Groof, Ad J. C.;Madra, Moneek;Ikenouchi, Junichi;Umeda, Masato;Bird, Thomas D.;Sturley, Stephen L.;Schon, Eric A.
通讯作者:
Schon, Eric A.
影响因子:
56.9
作者:
Chen, Jin;Brunner, Andreas-David;Weissman, Jonathan S.
通讯作者:
Weissman, Jonathan S.
DOI:
10.18632/aging.100943
发表时间:
2016-04
期刊:
Aging
影响因子:
--
作者:
Cobb LJ;Lee C;Xiao J;Yen K;Wong RG;Nakamura HK;Mehta HH;Gao Q;Ashur C;Huffman DM;Wan J;Muzumdar R;Barzilai N;Cohen P
通讯作者:
Cohen P