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Current thoughts on the role of mitochondria and free radicals in the biology of aging.关于线粒体和自由基在衰老生物学中的作用的当前观点。
J Gerontol A Biol Sci Med Sci. 2009 Feb;64(2):171-4. doi: 10.1093/gerona/gln058. Epub 2009 Jan 30.
2
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Complementary roles of mitochondrial respiration and ROS signaling on cellular aging and longevity.线粒体呼吸与活性氧信号在细胞衰老和寿命方面的互补作用。
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Cell senescence: an evaluation of replicative senescence in culture as a model for cell aging in situ.细胞衰老:对培养中的复制性衰老作为原位细胞衰老模型的评估。
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Age (Dordr). 2009 Dec;31(4):353-63. doi: 10.1007/s11357-009-9108-1.
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The aging oocyte--can mitochondrial function be improved?衰老的卵母细胞——线粒体功能可以改善吗?
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Tissue-specific reductions in mitochondrial efficiency and increased ROS release rates during ageing in zebra finches, Taeniopygia guttata.在斑马雀(Taeniopygia guttata)衰老过程中,组织特异性的线粒体效率降低和 ROS 释放率增加。
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Quality Matters? The Involvement of Mitochondrial Quality Control in Cardiovascular Disease.质量至关重要?线粒体质量控制在心血管疾病中的作用
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Mitochondrial DNA m.3243A > G heteroplasmy affects multiple aging phenotypes and risk of mortality.线粒体 DNA m.3243A>G 异质性影响多种衰老表型和死亡率风险。
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Age-related alterations in the sarcolemmal environment are attenuated by lifelong caloric restriction and voluntary exercise.终生热量限制和自主运动可减轻肌膜环境中与年龄相关的变化。
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Ageing-induced changes in the redox status of peripheral motor nerves imply an effect on redox signalling rather than oxidative damage.衰老引起的外周运动神经氧化还原状态变化意味着对氧化还原信号传导有影响,而非氧化损伤。
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Down-regulation of the mitochondrial matrix peptidase ClpP in muscle cells causes mitochondrial dysfunction and decreases cell proliferation.肌肉细胞中线粒体基质肽酶ClpP的下调会导致线粒体功能障碍并降低细胞增殖。
Free Radic Biol Med. 2016 Feb;91:281-92. doi: 10.1016/j.freeradbiomed.2015.12.021. Epub 2015 Dec 23.
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Modulation of the matrix redox signaling by mitochondrial Ca(2.).线粒体钙(Ca²⁺)对基质氧化还原信号的调节作用
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Mitochondrial DNA Heteroplasmy Associations With Neurosensory and Mobility Function in Elderly Adults.线粒体DNA异质性与老年人神经感觉和运动功能的关联
J Gerontol A Biol Sci Med Sci. 2015 Nov;70(11):1418-24. doi: 10.1093/gerona/glv097. Epub 2015 Aug 31.
10
Redox regulation of muscle adaptations to contractile activity and aging.肌肉对收缩活动和衰老适应的氧化还原调节
J Appl Physiol (1985). 2015 Aug 1;119(3):163-71. doi: 10.1152/japplphysiol.00760.2014. Epub 2015 Mar 19.

本文引用的文献

1
Overexpression of Mn superoxide dismutase does not increase life span in mice.锰超氧化物歧化酶的过表达不会延长小鼠的寿命。
J Gerontol A Biol Sci Med Sci. 2009 Nov;64(11):1114-25. doi: 10.1093/gerona/glp100. Epub 2009 Jul 24.
2
The overexpression of major antioxidant enzymes does not extend the lifespan of mice.主要抗氧化酶的过度表达并不会延长小鼠的寿命。
Aging Cell. 2009 Feb;8(1):73-5. doi: 10.1111/j.1474-9726.2008.00449.x. Epub 2008 Dec 11.
3
Life-long reduction in MnSOD activity results in increased DNA damage and higher incidence of cancer but does not accelerate aging.锰超氧化物歧化酶(MnSOD)活性的终身降低会导致DNA损伤增加和癌症发病率升高,但不会加速衰老。
Physiol Genomics. 2003 Dec 16;16(1):29-37. doi: 10.1152/physiolgenomics.00122.2003.
4
Aging: a theory based on free radical and radiation chemistry.衰老:一种基于自由基与辐射化学的理论。
J Gerontol. 1956 Jul;11(3):298-300. doi: 10.1093/geronj/11.3.298.
5
Ubiquitous overexpression of CuZn superoxide dismutase does not extend life span in mice.铜锌超氧化物歧化酶的普遍过表达不会延长小鼠的寿命。
J Gerontol A Biol Sci Med Sci. 2000 Jan;55(1):B5-9. doi: 10.1093/gerona/55.1.b5.
6
The biologic clock: the mitochondria?生物钟:线粒体?
J Am Geriatr Soc. 1972 Apr;20(4):145-7. doi: 10.1111/j.1532-5415.1972.tb00787.x.

Current thoughts on the role of mitochondria and free radicals in the biology of aging.

作者信息

Van Remmen Holly, Jones Dean P

机构信息

Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio, 15355 Lambda Drive, San Antonio, TX 78245-3207, USA.

出版信息

J Gerontol A Biol Sci Med Sci. 2009 Feb;64(2):171-4. doi: 10.1093/gerona/gln058. Epub 2009 Jan 30.

DOI:10.1093/gerona/gln058
PMID:19181714
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2655021/
Abstract
摘要