The role of mitochondrial dysfunction in age-related diseases

被引:161
|
作者
Lane, Rebecca K. [1 ]
Hilsabeck, Tyler [1 ,2 ]
Rea, Shane L. [1 ,3 ]
机构
[1] Univ Texas Hlth Sci Ctr San Antonio, Barshop Inst Longev & Aging Studies, San Antonio, TX 78245 USA
[2] Univ Texas San Antonio, San Antonio, TX 78249 USA
[3] Univ Texas Hlth Sci Ctr San Antonio, Dept Physiol, San Antonio, TX 78229 USA
来源
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS | 2015年 / 1847卷 / 11期
关键词
Mitochondria; Atherosclerosis; Neurodegeneration; Stem cells; Osteoporosis; Sirtuins; Immunity; Aging; LOW-DENSITY-LIPOPROTEIN; MESENCHYMAL STEM-CELLS; AMYLOID-BETA PEPTIDE; REACTIVE OXYGEN; OXIDATIVE STRESS; ALZHEIMERS-DISEASE; CYTOCHROME-C; MOUSE MODEL; POSTTRANSLATIONAL MODIFICATION; ANTIBACTERIAL ACTIVITY;
D O I
10.1016/j.bbabio.2015.05.021
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The aging process is accompanied by the onset of disease and a general decline in wellness. Insights into the aging process have revealed a number of cellular hallmarks of aging, among these epigenetic alterations, loss of proteostasis, mitochondrial dysfunction, cellular senescence, and stem cell exhaustion. Mitochondrial dysfunction increasingly appears to be a common factor connecting several of these hallmarks, driving the aging process and afflicting tissues throughout the body. Recent research has uncovered a much more complex involvement of mitochondria in the cell than has previously been appreciated and revealed novel ways in which mitochondrial defects feed into disease pathology. In this review we evaluate ways in which problems in mitochondria contribute to disease beyond the well-known mechanisms of oxidative stress and bioenergetic deficits, and we predict the direction that mitochondrial disease research will take in years to come. (c) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:1387 / 1400
页数:14
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