Oxidative Stress, Aging, and Short Peptides

被引:0
作者
Kuznik B.I. [1 ,2 ]
Linkova N.S. [3 ,4 ,5 ]
Ivko O.M. [3 ]
机构
[1] Department of Normal Physiology, Chita State Medical Academy, Ministry of Health of the Russian Federation, Chita
[2] “Health Academy” Innovation Clinic, Chita
[3] Department of Biogerontology, Research Center St. Petersburg Institute of Bioregulation and Gerontology, St. Petersburg
[4] Department of Therapy, Geriatrics, and Antiaging Medicine, Academy of Postgraduate Education, Federal Scientific and Clinical Center for Specialized Types of Medical Care and Medical Technologies, Federal Medical Biological Agency, Moscow
[5] “The Aging Challenge” Laboratory, Belgorod State National Research University, Belgorod
关键词
aging; neurodegenerative diseases; oxidative stress; short peptides;
D O I
10.1007/s11055-022-01219-1
中图分类号
学科分类号
摘要
This article reviews oxidative stress as one of the mechanisms impairing the functions of cells, organs, and tissues. Aging is associated with reductions in the activities of the enzymes of the antioxidant system. Reactive oxygen species formed in oxidant stress damage DNA, RNA, proteins, and lipids, leading to cell apoptosis. Neurodegenerative changes can develop in conditions of oxidant stress and mitochondrial dysfunction. A potential direction in the treatment of neurodegenerative pathology consists of using antioxidants such as melatonin or the short peptides AEDG and KE. Peptide AEDG stimulates endogenous melatonin synthesis as the body ages, while peptides AEDG and KE have antioxidant and geroprotective properties, normalizing telomere length and preventing cell apoptosis. Studies of oxidative stress at the cell, organ, and tissue levels are important for gerontology and the search for novel approaches to the treatment of neurodegenerative diseases. © 2022, Springer Science+Business Media, LLC, part of Springer Nature.
引用
收藏
页码:183 / 189
页数:6
相关论文
共 54 条
[21]  
Guo Y., Yu H., Leukocyte telomere length shortening and Alzheimer’s disease etiology, J. Alzheimers Dis., 69, 3, pp. 881-885, (2019)
[22]  
Hossain M.F., Uddin M.S., Uddin G.M.S., Et al., Melatonin in Alzheimer’s Disease: A latent endogenous regulator of neurogenesis to mitigate Alzheimer’s neuropathology, Mol. Neurobiol., 56, 12, pp. 8255-8276, (2019)
[23]  
Huang M.L., Chiang S., Kalinowski D.S., Et al., The role of the antioxidant response in mitochondrial dysfunction in degenerative diseases: cross-talk between antioxidant defense, autophagy, and apoptosis, Oxid. Med. Cell Longev., 2019, (2019)
[24]  
Huang T.T., Leu D., Zou Y., Oxidative stress and redox regulation on hippocampal-dependent cognitive functions, Arch. Biochem. Biophys., 576, pp. 2-7, (2015)
[25]  
Joshi G., Johnson J.A., The Nrf2-ARE pathway: A valuable therapeutic target for the treatment of neurodegenerative diseases, Recent Pat. CNS Drug Discov., 7, pp. 218-229, (2012)
[26]  
Kamat P.K., Kalani A., Rai S., Et al., Mechanism of oxidative stress and synapse dysfunction in the pathogenesis of Alzheimer’s Disease: Understanding the therapeutics strategies, Mol. Neurobiol., 53, 1, pp. 648-661, (2016)
[27]  
Kamat P.K., Rai S., Swarnkar S., Et al., Okadaic acid-induced tau phosphorylation in rat brain: role of NMDA receptor, Neuroscience, 238, pp. 97-113, (2013)
[28]  
Khavinson V.K., Bondarev I.E., Butyugov A.A., Smirnova T.D., Peptide promotes overcoming of the division limit in human somatic cell, Bull. Exp. Biol. Med., 137, 5, pp. 613-616, (2004)
[29]  
Khavinson V.K., Bondarev I.E., Butyugov A.A., Epithalon peptide induces telomerase activity and telomere elongation in human somatic cells, Bull. Exp. Biol. Med., 135, 6, pp. 590-592, (2003)
[30]  
Korovila I., Hugo M., Castro J.P., Et al., Proteostasis, oxidative stress and aging, Redox Biol., 13, pp. 550-567, (2017)