Morphometric examination of mitochondrial ultrastructure in aging cardiomyocytes

Eldarov, Chupalav; Vays, V. B.; Vangeli, I. M.; Kolosova, N. G.; Bakeeva, L. E.

doi:10.1134/s0006297915050132

Cited by 47 publications

(36 citation statements)

References 24 publications

(9 reference statements)

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“…For morphometric analysis of mitochondrial ultrastructure and of the average area of one mitochondrial section in the lacrimal gland, the Adobe ® Photoshop ® graphics editor was used for direct calculations, as described elsewhere [36-37]. …”

Section: Methodsmentioning

confidence: 99%

Mitochondria-targeted antioxidant SkQ1 reduces age-related alterations in the ultrastructure of the lacrimal gland

et al. 2016

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Dry eye syndrome is an eye disorder affecting many people at an old age. Because dry eye syndrome is accelerated by aging, a useful approach to the prevention of this syndrome may be an intervention into the aging process. Previously, we showed that the mitochondria-targeted antioxidant SkQ1 delays manifestations of aging and inhibits the development of age-related diseases including dry eye syndrome. Nevertheless, the link between SkQ1's effects and its suppression of age-related changes in the lacrimal gland remains unclear. Here we demonstrated that dietary supplementation with SkQ1 (250 nmol/[kg body weight] daily) starting at age 1.5 months significantly alleviated the pathological changes in lacrimal glands of Wistar rats by age 24 months. By this age, lacrimal glands underwent dramatic deterioration of the ultrastructure that was indicative of irreversible disturbances in these glands' functioning. In contrast, in SkQ1-treated rats, the ultrastructure of the lacrimal gland was similar to that in much younger rats. Morphometric analysis of electron-microscopic specimens of lacrimal glands revealed the presence of numerous secretory granules in acinar cells and a significant increase in the number of operating intercalary ducts. Our results confirm that dietary supplementation with SkQ1 is a promising approach to healthy ageing and to prevention of aberrations in the lacrimal gland that underlie dry eye syndrome.

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Section: Methodsmentioning

confidence: 99%

Mitochondria-targeted antioxidant SkQ1 reduces age-related alterations in the ultrastructure of the lacrimal gland

et al. 2016

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“…Whereas some studies demonstrate a reduced number of mitochondria in the cytosol of aged cardiomyocytes, others show that the mitochondrial volume fraction is unaltered during ageing . Mitochondrial shape is altered with increasing age (less elongated and more round), and the area of the mitochondrial inner membrane per mitochondrion is reduced in aged myocardium although cristae configuration is not affected …”

Section: Age‐associated Changes In the Heartmentioning

confidence: 98%

Mitochondria and ageing: role in heart, skeletal muscle and adipose tissue

Boengler

Kosiol

Mayr

et al. 2017

J cachexia sarcopenia muscle

313

191

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Age is the most important risk factor for most diseases. Mitochondria play a central role in bioenergetics and metabolism. In addition, several lines of evidence indicate the impact of mitochondria in lifespan determination and ageing. The best‐known hypothesis to explain ageing is the free radical theory, which proposes that cells, organs, and organisms age because they accumulate reactive oxygen species (ROS) damage over time. Mitochondria play a central role as the principle source of intracellular ROS, which are mainly formed at the level of complex I and III of the respiratory chain. Dysfunctional mitochondria generating less ATP have been observed in various aged organs. Mitochondrial dysfunction comprises different features including reduced mitochondrial content, altered mitochondrial morphology, reduced activity of the complexes of the electron transport chain, opening of the mitochondrial permeability transition pore, and increased ROS formation. Furthermore, abnormalities in mitochondrial quality control or defects in mitochondrial dynamics have also been linked to senescence. Among the tissues affected by mitochondrial dysfunction are those with a high‐energy demand and thus high mitochondrial content. Therefore, the present review focuses on the impact of mitochondria in the ageing process of heart and skeletal muscle. In this article, we review different aspects of mitochondrial dysfunction and discuss potential therapeutic strategies to improve mitochondrial function. Finally, novel aspects of adipose tissue biology and their involvement in the ageing process are discussed.

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“…Evidence suggests that the mitochondria structure is disrupted in cardiac senescence, with increased mitochondria size [34]. Electron-microscopy-based studies have demonstrated that the area of IMM obviously decreases [35], showing a loss of cristae with age in rodent heart [36]. Mitochondrial dynamics have been involved in the aging process [37], and the promotion of fusion or blockade of fission prompts cell senescence [17].…”

Section: Mitochondrial Dysfunction In Cardiac Agingmentioning

confidence: 99%

Mitochondrial ROS-Modulated mtDNA: A Potential Target for Cardiac Aging

Quan

Xin

Tian

et al. 2020

Oxidative Medicine and Cellular Longevity

134

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Mitochondrial DNA (mtDNA) damage is associated with the development of cardiovascular diseases. Cardiac aging plays a central role in cardiovascular diseases. There is accumulating evidence linking cardiac aging to mtDNA damage, including mtDNA mutation and decreased mtDNA copy number. Current wisdom indicates that mtDNA is susceptible to damage by mitochondrial reactive oxygen species (mtROS). This review presents the cellular and molecular mechanisms of cardiac aging, including autophagy, chronic inflammation, mtROS, and mtDNA damage, and the effects of mitochondrial biogenesis and oxidative stress on mtDNA. The importance of nucleoid-associated proteins (Pol γ), nuclear respiratory factors (NRF1 and NRF2), the cGAS-STING pathway, and the mitochondrial biogenesis pathway concerning the development of mtDNA damage during cardiac aging is discussed. Thus, the repair of damaged mtDNA provides a potential clinical target for preventing cardiac aging.

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Morphometric examination of mitochondrial ultrastructure in aging cardiomyocytes

Cited by 47 publications

References 24 publications

Mitochondria-targeted antioxidant SkQ1 reduces age-related alterations in the ultrastructure of the lacrimal gland

Mitochondria-targeted antioxidant SkQ1 reduces age-related alterations in the ultrastructure of the lacrimal gland

Mitochondria and ageing: role in heart, skeletal muscle and adipose tissue

Mitochondrial ROS-Modulated mtDNA: A Potential Target for Cardiac Aging

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