Mitochondrial pathways in human health and aging

被引：53

作者：

Bornstein, Rebecca ^{[1
]}

Gonzalez, Brenda ^{[2
]}

Johnson, Simon C. ^{[3
,4
,5
]}

机构：

[1] Univ Washington, Dept Pathol, Seattle, WA 98195 USA

[2] Albert Einstein Coll Med, Dept Genet, Bronx, NY 10467 USA

[3] Univ Washington, Dept Neurol, Seattle, WA 98195 USA

[4] Univ Washington, Dept Anesthesiol & Pain Med, Seattle, WA 98195 USA

[5] Seattle Childrens Res Inst, Ctr Integrat Brain Res, Seattle, WA USA

来源：

MITOCHONDRION | 2020年 / 54卷

关键词：

UNFOLDED PROTEIN RESPONSE; LIFE-SPAN EXTENSION; FREE-RADICAL THEORY; DNA MUTATIONS; OXIDATIVE STRESS; SKELETAL-MUSCLE; QUALITY-CONTROL; MOLECULAR-MECHANISMS; UNCOUPLING PROTEIN-3; RETROGRADE RESPONSE;

D O I：

10.1016/j.mito.2020.07.007

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Mitochondria are eukaryotic organelles known best for their roles in energy production and metabolism. While often thought of as simply the 'powerhouse of the cell,' these organelles participate in a variety of critical cellular processes including reactive oxygen species (ROS) production, regulation of programmed cell death, modulation of inter- and intracellular nutrient signaling pathways, and maintenance of cellular proteostasis. Disrupted mitochondrial function is a hallmark of eukaryotic aging, and mitochondrial dysfunction has been reported to play a role in many aging-related diseases. While mitochondria are major players in human diseases, significant questions remain regarding their precise mechanistic role. In this review, we detail mechanisms by which mitochondrial dysfunction participate in disease and aging based on findings from model organisms and human genetics studies.

引用

页码：72 / 84

页数：13

共 181 条

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