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  1. Article ; Online: Calculating Aging: Analysis of Survival Curves in the Norm and Pathology, Fluctuations in Mortality Dynamics, Characteristics of Lifespan Distribution, and Indicators of Lifespan Variation.

    Shilovsky, Gregory A

    Biochemistry. Biokhimiia

    2024  Volume 89, Issue 2, Page(s) 371–376

    Abstract: The article describes the history of studies of survival data carried out at the Research Institute of Physico-Chemical Biology under the leadership of Academician V. P. Skulachev from 1970s until present, with special emphasis on the last decade. The ... ...

    Abstract The article describes the history of studies of survival data carried out at the Research Institute of Physico-Chemical Biology under the leadership of Academician V. P. Skulachev from 1970s until present, with special emphasis on the last decade. The use of accelerated failure time (AFT) model and analysis of coefficient of variation of lifespan (CV
    MeSH term(s) Humans ; Longevity/physiology ; Aging/genetics ; Mutation ; Oxidative Stress
    Language English
    Publishing date 2024-03-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1109-5
    ISSN 1608-3040 ; 0006-2979 ; 0320-9717
    ISSN (online) 1608-3040
    ISSN 0006-2979 ; 0320-9717
    DOI 10.1134/S0006297924020159
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Lability of the Nrf2/Keap/ARE Cell Defense System in Different Models of Cell Aging and Age-Related Pathologies.

    Shilovsky, Gregory A

    Biochemistry. Biokhimiia

    2022  Volume 87, Issue 1, Page(s) 70–85

    Abstract: The level of oxidative stress in an organism increases with age. Accumulation of damages resulting in the disruption of genome integrity can be the cause of many age-related diseases and appearance of phenotypic and physiological signs of aging. In this ... ...

    Abstract The level of oxidative stress in an organism increases with age. Accumulation of damages resulting in the disruption of genome integrity can be the cause of many age-related diseases and appearance of phenotypic and physiological signs of aging. In this regard, the Nrf2 system, which regulates expression of numerous enzymes responsible for the antioxidant defense and detoxification, is of great interest. This review summarizes and analyzes the data on the age-related changes in the Nrf2 system in vivo and in vitro in various organs and tissues. Analysis of published data suggests that the capacity for Nrf2 activation (triggered by the increased level of oxidative stress) steadily declines with age. At the same time, changes in the Nrf2 activity under the stress-free conditions do not have such unambiguous directionality; in many studies, these changes were statistically insignificant, although it is commonly accepted that the level of oxidative stress steadily increases with aging. This review examines the role of cell regulatory systems limiting the ability of Nrf2 to respond to oxidative stress. Senescent cells are extremely susceptible to the oxidative damage due to the impaired Nrf2 signaling. Activation of the Nrf2 pathway is a promising target for new pharmacological or genetic therapeutic strategies. Suppressors of the Nrf2 expression, such as Keap1, GSK3, c-Myc, and Bach1, may contribute to the age-related impairments in the induction of Nrf2-regulated antioxidant genes. Understanding the mechanisms of regulatory cascades linking the programs responsible for the maintenance of homeostasis and cell response to the oxidative stress will contribute to the elucidation of molecular mechanisms underlying aging and longevity.
    MeSH term(s) Antioxidants/metabolism ; Cellular Senescence ; Glycogen Synthase Kinase 3/metabolism ; Kelch-Like ECH-Associated Protein 1 ; NF-E2-Related Factor 2/metabolism
    Chemical Substances Antioxidants ; Kelch-Like ECH-Associated Protein 1 ; NF-E2-Related Factor 2 ; Glycogen Synthase Kinase 3 (EC 2.7.11.26)
    Language English
    Publishing date 2022-04-28
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1109-5
    ISSN 1608-3040 ; 0006-2979 ; 0320-9717
    ISSN (online) 1608-3040
    ISSN 0006-2979 ; 0320-9717
    DOI 10.1134/S0006297922010060
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  3. Article ; Online: Variability of Mortality: Additional Information on Mortality and Morbidity Curves under Normal and Pathological Conditions [Commentary on the Article by A. G. Malygin "Programmed Risks of Death in Male Patients with Diabetes" Published in Biochemistry (Moscow), vol. 86, pp. 1553-1562 (2021)].

    Shilovsky, Gregory A

    Biochemistry. Biokhimiia

    2022  Volume 87, Issue 3, Page(s) 294–299

    Abstract: Analysis of demographic data indicates uneven distribution of mortality within a year, month, and even week time period. This is of great practical importance for the operation of medical institutions, including intensive care units, and makes it ... ...

    Abstract Analysis of demographic data indicates uneven distribution of mortality within a year, month, and even week time period. This is of great practical importance for the operation of medical institutions, including intensive care units, and makes it possible to calculate economic and labor requirements of medical institutions. All the above is especially relevant during the era of the COVID-19 pandemic. Malygin showed the presence of one to two fluctuations per week in the mortality of male patients with type 2 diabetes. The height of the peaks of such fluctuations is determined, as expected, by the regular parameter indicating their position on the axis of lifespan and random parameter reflecting adverse effects of external environmental factors on the body, as well as the extent of the periodically occurring sharp decrease in the nonspecific resistance. This article discusses results of recent research in the field of small (semi-weekly, weekly, monthly, and seasonal) fluctuations of mortality. Based on a large array of accumulated data, it can be concluded that the decrease in seasonal variability of mortality accompanies an increase in the life expectancy. Studying characteristics of mortality fluctuations makes it possible to move from investigating the impact of biorhythms (Master Clock) on the development of acute and chronic phenoptotic processes directly to studying the patterns of mortality rhythms themselves (rhythms of phenoptosis).
    MeSH term(s) COVID-19 ; Diabetes Mellitus, Type 2 ; Humans ; Male ; Morbidity ; Moscow ; Pandemics
    Language English
    Publishing date 2022-05-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1109-5
    ISSN 1608-3040 ; 0006-2979 ; 0320-9717
    ISSN (online) 1608-3040
    ISSN 0006-2979 ; 0320-9717
    DOI 10.1134/S0006297922030087
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Regulation of Cell Proliferation and Nrf2-Mediated Antioxidant Defense: Conservation of Keap1 Cysteines and Nrf2 Binding Site in the Context of the Evolution of KLHL Family.

    Shilovsky, Gregory A / Dibrova, Daria V

    Life (Basel, Switzerland)

    2023  Volume 13, Issue 4

    Abstract: Keap1 (Kelch-like ECH-associated protein 1) is one of the major negative regulators of the transcription factor Nrf2 (nuclear factor erythroid-2-related factor 2), which induces the expression of numerous proteins defending the cell against different ... ...

    Abstract Keap1 (Kelch-like ECH-associated protein 1) is one of the major negative regulators of the transcription factor Nrf2 (nuclear factor erythroid-2-related factor 2), which induces the expression of numerous proteins defending the cell against different stress conditions. Keap1 is generally negatively regulated by post-translational modification (mostly via its cysteine residues) and interaction with other proteins that compete with Nrf2 for binding. Cysteine residues in Keap1 have different effects on protein regulation, as basic residues (Lys, Arg, and His) in close proximity to them increase cysteine modification potential. In this paper, we present an evolutionary analysis of residues involved in both mechanisms of Keap1 regulation in the broader context of the KLHL protein family in vertebrates. We identified the typical domain structure of the KLHL protein family in several proteins outside of this family (namely in KBTBD proteins 2, 3, 4, 6, 7, 8, 12 and 14). We found several cysteines that are flanked by basic residues (namely, C14, C38, C151, C226, C241, C273, C288, C297, C319, and C613) and, therefore, may be considered more susceptible to regulatory modification. The Nrf2 binding site is completely conserved in Keap1 in vertebrates but is absent or located in nonaligned DA and BC loops of the Kelch domain within the KLHL family. The development of specific substrate binding regions could be an evolutionary factor of diversification in the KLHL protein family.
    Language English
    Publishing date 2023-04-19
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2662250-6
    ISSN 2075-1729
    ISSN 2075-1729
    DOI 10.3390/life13041045
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Transcription Factor Nrf2 and Mitochondria - Friends or Foes in the Regulation of Aging Rate.

    Shilovsky, Gregory A / Ashapkin, Vasily V

    Biochemistry. Biokhimiia

    2023  Volume 87, Issue 12, Page(s) 1477–1486

    Abstract: At the first sight, the transcription factor Nrf2 as a master regulator of cellular antioxidant systems, and mitochondria as the main source of reactive oxygen species (ROS), should play the opposite roles in determining the pace of aging. However, since ...

    Abstract At the first sight, the transcription factor Nrf2 as a master regulator of cellular antioxidant systems, and mitochondria as the main source of reactive oxygen species (ROS), should play the opposite roles in determining the pace of aging. However, since the causes of aging cannot be confined to the oxidative stress, the role of Nrf2 role cannot be limited to the regulation of antioxidant systems, and moreover, the role of mitochondria is not confined to the ROS production. In this review, we discussed only one aspect of this problem, namely, the molecular mechanisms of interaction between Nrf2 and mitochondria that influence the rate of aging and the lifespan. Experimental data accumulated so far show that the Nrf2 activity positively affects both the mitochondrial dynamics and mitochondrial quality control. Nrf2 influences the mitochondrial function through various mechanisms, e.g., regulation of nuclear genome-encoded mitochondrial proteins and changes in the balance of ROS or other metabolites that affect the functioning of mitochondria. In turn, multiple regulatory proteins functionally associated with the mitochondria affect the Nrf2 activity and even form mutual regulatory loops with Nrf2. We believe that these loops enable the fine-tuning of the cellular redox balance and, possibly, of the cellular metabolism as a whole. It has been commonly accepted for a long time that all mitochondrial regulatory signals are mediated by the nuclear genome-encoded proteins, whereas the mitochondrial genome encodes only a few respiratory chain proteins and two ribosomal RNAs. Relatively recently, mtDNA-encoded signal peptides have been discovered. In this review, we discuss the data on their interactions with the nuclear regulatory systems, first of all, Nrf2, and their possible involvement in the regulation of the aging rate. The interactions between regulatory cascades that link the programs ensuring the maintenance of cellular homeostasis and cellular responses to the oxidative stress are a significant part of both aging and anti-aging programs. Therefore, understanding these interactions will be of great help in searching for the molecular targets to counteract aging-associated diseases and aging itself.
    MeSH term(s) Humans ; Antioxidants/metabolism ; Reactive Oxygen Species/metabolism ; NF-E2-Related Factor 2/metabolism ; Oxidative Stress/physiology ; Mitochondria/metabolism ; Aging
    Chemical Substances Antioxidants ; Reactive Oxygen Species ; NF-E2-Related Factor 2
    Language English
    Publishing date 2023-01-30
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1109-5
    ISSN 1608-3040 ; 0006-2979 ; 0320-9717
    ISSN (online) 1608-3040
    ISSN 0006-2979 ; 0320-9717
    DOI 10.1134/S0006297922120057
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  6. Article ; Online: Evolution of Longevity in Tetrapods: Safety Is More Important than Metabolism Level.

    Shilovsky, Gregory A / Putyatina, Tatyana S / Markov, Alexander V

    Biochemistry. Biokhimiia

    2024  Volume 89, Issue 2, Page(s) 322–340

    Abstract: Various environmental morphological and behavioral factors can determine the longevity of representatives of various taxa. Long-lived species develop systems aimed at increasing organism stability, defense, and, ultimately, lifespan. Long-lived species ... ...

    Abstract Various environmental morphological and behavioral factors can determine the longevity of representatives of various taxa. Long-lived species develop systems aimed at increasing organism stability, defense, and, ultimately, lifespan. Long-lived species to a different extent manifest the factors favoring longevity (gerontological success), such as body size, slow metabolism, activity of body's repair and antioxidant defense systems, resistance to toxic substances and tumorigenesis, and presence of neotenic features. In continuation of our studies of mammals, we investigated the characteristics that distinguish long-lived ectotherms (crocodiles and turtles) and compared them with those of other ectotherms (squamates and amphibians) and endotherms (birds and mammals). We also discussed mathematical indicators used to assess the predisposition to longevity in different species, including standard indicators (mortality rate, maximum lifespan, coefficient of variation of lifespan) and their derivatives. Evolutionary patterns of aging are further explained by the protective phenotypes and life history strategies. We assessed the relationship between the lifespan and various studied factors, such as body size and temperature, encephalization, protection of occupied ecological niches, presence of protective structures (for example, shells and osteoderms), and environmental temperature, and the influence of these factors on the variation of the lifespan as a statistical parameter. Our studies did not confirm the hypothesis on the metabolism level and temperature as the most decisive factors of longevity. It was found that animals protected by shells (e.g., turtles with their exceptional longevity) live longer than species that have poison or lack such protective adaptations. The improvement of defense against external threats in long-lived ectotherms is consistent with the characteristics of long-lived endotherms (for example, naked mole-rats that live in underground tunnels, or bats and birds, whose ability to fly is one of the best defense mechanisms).
    MeSH term(s) Animals ; Longevity ; Aging ; Oxidative Stress ; Antioxidants ; Mammals
    Chemical Substances Antioxidants
    Language English
    Publishing date 2024-03-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1109-5
    ISSN 1608-3040 ; 0006-2979 ; 0320-9717
    ISSN (online) 1608-3040
    ISSN 0006-2979 ; 0320-9717
    DOI 10.1134/S0006297924020111
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Evolution of Longevity as a Species-Specific Trait in Mammals.

    Shilovsky, Gregory A / Putyatina, Tatyana S / Markov, Alexander V

    Biochemistry. Biokhimiia

    2023  Volume 87, Issue 12, Page(s) 1579–1599

    Abstract: From the evolutionary point of view, the priority problem for an individual is not longevity, but adaptation to the environment associated with the need for survival, food supply, and reproduction. We see two main vectors in the evolution of mammals. One ...

    Abstract From the evolutionary point of view, the priority problem for an individual is not longevity, but adaptation to the environment associated with the need for survival, food supply, and reproduction. We see two main vectors in the evolution of mammals. One is a short lifespan and numerous offspring ensuring reproductive success (r-strategy). The other one is development of valuable skills in order compete successfully (K-strategy). Species with the K-strategy should develop and enhance specific systems (anti-aging programs) aimed at increasing the reliability and adaptability, including lifespan. These systems are signaling cascades that provide cell repair and antioxidant defense. Hence, any arbitrarily selected long-living species should be characterized by manifestation to a different extent of the longevity-favoring traits (e.g., body size, brain development, sociality, activity of body repair and antioxidant defense systems, resistance to xenobiotics and tumor formation, presence of neotenic traits). Hereafter, we will call a set of such traits as the gerontological success of a species. Longevity is not equivalent to the evolutionary or reproductive success. This difference between these phenomena reaches its peak in mammals due to the development of endothermy and cephalization associated with the cerebral cortex expansion, which leads to the upregulated production of oxidative radicals by the mitochondria (and, consequently, accelerated aging), increase in the number of non-dividing differentiated cells, accumulation of the age-related damage in these cells, and development of neurodegenerative diseases. The article presents mathematical indicators used to assess the predisposition to longevity in different species (including the standard mortality rate and basal metabolic rate, as well as their derivatives). The properties of the evolution of mammals (including the differences between modern mammals and their ancestral forms) are also discussed.
    MeSH term(s) Animals ; Longevity ; Antioxidants ; Reproducibility of Results ; Aging/metabolism ; Mammals
    Chemical Substances Antioxidants
    Language English
    Publishing date 2023-01-31
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1109-5
    ISSN 1608-3040 ; 0006-2979 ; 0320-9717
    ISSN (online) 1608-3040
    ISSN 0006-2979 ; 0320-9717
    DOI 10.1134/S0006297922120148
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Altruism and Phenoptosis as Programs Supported by Evolution.

    Shilovsky, Gregory A / Putyatina, Tatyana S / Markov, Alexander V

    Biochemistry. Biokhimiia

    2021  Volume 86, Issue 12, Page(s) 1540–1552

    Abstract: Phenoptosis is a programmed death that has emerged in the process of evolution, sometimes taking the form of an altruistic program. In particular, it is believed to be a weapon against the spread of pandemics in the past and an obstacle in fighting ... ...

    Abstract Phenoptosis is a programmed death that has emerged in the process of evolution, sometimes taking the form of an altruistic program. In particular, it is believed to be a weapon against the spread of pandemics in the past and an obstacle in fighting pandemics in the present (COVID). However, on the evolutionary scale, deterministic death is not associated with random relationships (for example, bacteria with a particular mutation), but is a product of higher nervous activity or a consequence of established hierarchy that reaches its maximal expression in eusocial communities of Hymenoptera and highly social communities of mammals. Unlike a simple association of individuals, eusociality is characterized by the appearance of non-reproductive individuals as the highest form of altruism. In contrast to primitive programs for unicellular organisms, higher multicellular organisms are characterized by the development of behavior-based phenoptotic programs, especially in the case of reproduction-associated limitation of lifespan. Therefore, we can say that the development of altruism in the course of evolution of sociality leads in its extreme manifestation to phenoptosis. Development of mathematical models for the emergence of altruism and programmed death contributes to our understanding of mechanisms underlying these paradoxical counterproductive (harmful) programs. In theory, this model can be applied not only to insects, but also to other social animals and even to the human society. Adaptive death is an extreme form of altruism. We consider altruism and programmed death as programmed processes in the mechanistic and adaptive sense, respectively. Mechanistically, this is a program existing as a predetermined chain of certain responses, regardless of its adaptive value. As to its adaptive value (regardless of the degree of "phenoptoticity"), this is a characteristic of organisms that demonstrate high levels of kinship, social organization, and physical association typical for higher-order individuals, e.g., unicellular organisms forming colonies with some characteristics of multicellular animals or colonies of multicellular animals displaying features of supraorganisms.
    MeSH term(s) Altruism ; Animals ; Apoptosis ; Biological Evolution ; COVID-19 ; Humans ; Insecta/physiology ; SARS-CoV-2
    Language English
    Publishing date 2021-12-22
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1109-5
    ISSN 1608-3040 ; 0006-2979 ; 0320-9717
    ISSN (online) 1608-3040
    ISSN 0006-2979 ; 0320-9717
    DOI 10.1134/S0006297921120038
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  9. Article ; Online: Effect of Caloric Restriction on Aging: Fixing the Problems of Nutrient Sensing in Postmitotic Cells?

    Morgunova, Galina V / Shilovsky, Gregory A / Khokhlov, Alexander N

    Biochemistry. Biokhimiia

    2021  Volume 86, Issue 10, Page(s) 1352–1367

    Abstract: The review discusses the role of metabolic disorders (in particular, insulin resistance) in the development of age-related diseases and normal aging with special emphasis on the changes in postmitotic cells of higher organisms. Caloric restriction helps ... ...

    Abstract The review discusses the role of metabolic disorders (in particular, insulin resistance) in the development of age-related diseases and normal aging with special emphasis on the changes in postmitotic cells of higher organisms. Caloric restriction helps to prevent such metabolic disorders, which could probably explain its ability to prolong the lifespan of laboratory animals. Maintaining metabolic homeostasis is especially important for the highly differentiated long-lived body cells, whose lifespan is comparable to the lifespan of the organism itself. Normal functioning of these cells can be ensured only upon correct functioning of the cytoplasm clean-up system and availability of all required nutrients and energy sources. One of the central problems in gerontology is the age-related disruption of glucose metabolism leading to obesity, diabetes, metabolic syndrome, and other related pathologies. Along with the adipose tissue, skeletal muscles are the main consumers of insulin; hence the physical activity of muscles, which supports their energy metabolism, delays the onset of insulin resistance. Insulin resistance disrupts the metabolism of cardiomyocytes, so that they fail to utilize the nutrients to perform their functions even being surrounded by a nutrient-rich environment, which contributes to the development of age-related cardiovascular diseases. Metabolic pathologies also alter the nutrient sensitivity of neurons, thus disrupting the action of insulin in the central nervous system. In addition, there is evidence that neurons can develop insulin resistance as well. It has been suggested that affecting nutritional sensors (e.g., AMPK) in postmitotic cells might improve the state of the entire multicellular organism, slow down its aging, and increase the lifespan.
    MeSH term(s) AMP-Activated Protein Kinases/metabolism ; Aging/metabolism ; Animals ; Caloric Restriction/methods ; Energy Metabolism ; Homeostasis ; Humans ; Longevity ; Metabolic Diseases/pathology ; Metabolic Diseases/prevention & control ; Mitosis ; Nutrients/metabolism
    Chemical Substances AMP-Activated Protein Kinases (EC 2.7.11.31)
    Language English
    Publishing date 2021-12-10
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1109-5
    ISSN 1608-3040 ; 0006-2979 ; 0320-9717
    ISSN (online) 1608-3040
    ISSN 0006-2979 ; 0320-9717
    DOI 10.1134/S0006297921100151
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Six Functions of Respiration: Isn't It Time to Take Control over ROS Production in Mitochondria, and Aging Along with It?

    Skulachev, Vladimir P / Vyssokikh, Mikhail Yu / Chernyak, Boris V / Mulkidjanian, Armen Y / Skulachev, Maxim V / Shilovsky, Gregory A / Lyamzaev, Konstantin G / Borisov, Vitaliy B / Severin, Fedor F / Sadovnichii, Victor A

    International journal of molecular sciences

    2023  Volume 24, Issue 16

    Abstract: Cellular respiration is associated with at least six distinct but intertwined biological functions. (1) biosynthesis of ATP from ADP and inorganic phosphate, (2) consumption of respiratory substrates, (3) support of membrane transport, (4) conversion of ... ...

    Abstract Cellular respiration is associated with at least six distinct but intertwined biological functions. (1) biosynthesis of ATP from ADP and inorganic phosphate, (2) consumption of respiratory substrates, (3) support of membrane transport, (4) conversion of respiratory energy to heat, (5) removal of oxygen to prevent oxidative damage, and (6) generation of reactive oxygen species (ROS) as signaling molecules. Here we focus on function #6, which helps the organism control its mitochondria. The ROS bursts typically occur when the mitochondrial membrane potential (MMP) becomes too high, e.g., due to mitochondrial malfunction, leading to cardiolipin (CL) oxidation. Depending on the intensity of CL damage, specific programs for the elimination of damaged mitochondria (mitophagy), whole cells (apoptosis), or organisms (phenoptosis) can be activated. In particular, we consider those mechanisms that suppress ROS generation by enabling ATP synthesis at low MMP levels. We discuss evidence that the mild depolarization mechanism of direct ATP/ADP exchange across mammalian inner and outer mitochondrial membranes weakens with age. We review recent data showing that by protecting CL from oxidation, mitochondria-targeted antioxidants decrease lethality in response to many potentially deadly shock insults. Thus, targeting ROS- and CL-dependent pathways may prevent acute mortality and, hopefully, slow aging.
    MeSH term(s) Animals ; Reactive Oxygen Species ; Respiration ; Mitochondria ; Aging ; Cardiolipins ; Adenosine Triphosphate ; Mammals
    Chemical Substances Reactive Oxygen Species ; Cardiolipins ; Adenosine Triphosphate (8L70Q75FXE)
    Language English
    Publishing date 2023-08-08
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms241612540
    Database MEDical Literature Analysis and Retrieval System OnLINE

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