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Review
. 2020 Jul 7;8(7):198.
doi: 10.3390/biomedicines8070198.

The Link between Chronic Stress and Accelerated Aging

Yegor E Yegorov  1 , Anastasia V Poznyak  2 , Nikita G Nikiforov  3   4   5 , Igor A Sobenin  3 , Alexander N Orekhov  2   5   6
Affiliations
Review

The Link between Chronic Stress and Accelerated Aging

Yegor E Yegorov et al. Biomedicines. .

Abstract

People exposed to chronic stress age rapidly. The telomeres in their cells of all types shorten faster. Inflammation is another important feature of stress that, along with aging, accounts for the phenomenon of inflammaging. In addition to aging itself, inflammaging can contribute to the development of several pathologies, including atherosclerosis, diabetes, hypertension, and others. Oxidative stress is one of the main mechanisms related to stress. Oxidative stress is caused by the over-production of reactive oxygen species (ROS) that can damage various tissues. The main source of ROS is mitochondria. Being suppressed by mitochondrial mutations, mitophagy can aggravate the situation. In this case, the aging-specific pro-inflammatory changes are amplified. It happens because of the inability of cells to maintain the normal state of mitochondria. Macrophages are the crucial element of the innate immunity associated with the chronic inflammation and, subsequently, with the inflammaging. In this review, we focus on the therapy approaches potentially reducing the deleterious effects of oxidative stress. These include stimulation of mitophagy, activation of mitochondrial uncoupling, induction of the expression of the telomerase catalytic component gene, and use of antioxidants. Any method reducing oxidative stress should improve post-traumatic stress disorder.

Keywords: ROS; antioxidants; inflammaging; macrophage; mitochondria; mitophagy; oxidative stress; uncoupling.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Scheme of the association between psychological stress and inflammaging through oxidative stress; potential interventions to reduce the resulting detrimental effects are listed on the right.
Figure 2
Figure 2
Generation of reactive oxygen species (ROS) by the mitochondrial respiratory chain. Superoxide anions generated by the respiratory chain damage the respiratory chain itself and the mitochondrial DNA, which leads to changes in the respiratory chain that increase the production of the superoxide anion. Superoxide anions also damage the mitochondrial membranes, causing lipid peroxidation and leading to changes in membrane properties. Special superoxide dismutase (SOD) enzymes convert superoxide anions into hydrogen peroxide, which is then converted to water by peroxiredoxins (Prx) and glutathione peroxidase (GPx). Hydrogen peroxide plays a major redox-regulating (RR) role in this system. In mitochondria, it changes the activity of enzymes, in the cytosol, it affects the delivery of substrates into the mitochondria, whereas, in the nucleus, it alters the activity of transcription factors, causing the response kernel, which is reflected in increased protein expression of uncouplers (UCPs). UCPs are transported to the mitochondria, where they reduce the proton potential of the inner membrane, thereby reducing the production of the superoxide anion. Excessive production of hydrogen peroxide in the cytoplasm triggers autophagy processes, causes shortening of telomeres, potentially starts the process of apoptosis and causes increased expression of pro-inflammatory factors that can affect neighboring cells and the whole organism [27].
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