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Mitochondria: Aging, Metabolic Syndrome and Cardiovascular Diseases
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Mitochondria: Aging, Metabolic Syndrome and Cardiovascular Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (30 September 2022) | Viewed by 10023

Special Issue Editor

Dr. Alexander Panov

E-Mail Website
Guest Editor
Federal Scientific Center for Family Health and Human Reproduction Problems, 16 Timiryasev Str., 664003 Irkutsk, Russia
Interests: mitochondria; metabolism; ROS; oxidative stress; aging mechanisms; metabolic gender diversity; metabolic syndrome; ontogenesis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The three major biomedical problems, aging, metabolic syndrome, and cardiovascular diseases, have a long history of research. The scientists working on these problems that are vital for human health after the years of studies have concluded that dysfunctions of mitochondria and associated metabolic aberrations lie at the center of these biomedical problems. Additionally, the medical problems of old age, metabolic syndrome, and cardiovascular dysfunctions usually appear at the transition from the reproductive to the postreproductive stage of the human postembryonic ontogenesis. We invite specialists working in these fields to share their observations and new ideas regarding the involvement of mitochondrial dysfunctions in the mechanisms of aging, the development of metabolic syndrome, and cardiovascular pathologies. We hope that combining current views and facts from different perspectives will promote our understanding of the main common mechanisms underlying these medical problems.

Dr. Alexander Panov
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Published Papers (3 papers)

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Research

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13 pages, 1353 KiB  
Article
Functional State of Rat Heart Mitochondria in Experimental Hyperthyroidism
by Natalya Venediktova, Ilya Solomadin, Anna Nikiforova, Vlada Starinets and Galina Mironova
Int. J. Mol. Sci. 2021, 22(21), 11744; https://doi.org/10.3390/ijms222111744 - 29 Oct 2021
Cited by 9 | Viewed by 1705
Abstract
In this work, the effect of thyroxine on energy and oxidative metabolism in the mitochondria of the rat heart was studied. Hyperthyroidism was observed in experimental animals after chronic administration of T4, which was accompanied by an increase in serum concentrations [...] Read more.
In this work, the effect of thyroxine on energy and oxidative metabolism in the mitochondria of the rat heart was studied. Hyperthyroidism was observed in experimental animals after chronic administration of T4, which was accompanied by an increase in serum concentrations of free triiodothyronine (T3) and thyroxine (T4) by 1.8 and 3.4 times, respectively. The hyperthyroid rats (HR) had hypertrophy of the heart. In HR, there was a change in the oxygen consumption in the mitochondria of the heart, especially when using palmitoylcarnitine. The assay of respiratory chain enzymes revealed that the activities of complexes I, I + III, III, IV increased, whereas the activities of complexes II, II + III decreased in heart mitochondria of the experimental animals. It was shown that the level of respiratory complexes of the electron transport chain in hyperthyroid rats increased, except for complex V, the quantity of which was reduced. The development of oxidative stress in HR was observed: an increase in the hydrogen peroxide production rate, increase in lipid peroxidation and reduced glutathione. The activity of superoxide dismutase in the heart of HR was higher than in the control. At the same time, the activity of glutathione peroxidase decreased. The obtained data indicate that increased concentrations of thyroid hormones lead to changes in energy metabolism and the development of oxidative stress in the heart of rats, which in turn contributes to heart dysfunction. Full article
(This article belongs to the Special Issue Mitochondria: Aging, Metabolic Syndrome and Cardiovascular Diseases)
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Review

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19 pages, 1551 KiB  
Review
Metabolic Syndrome and β-Oxidation of Long-Chain Fatty Acids in the Brain, Heart, and Kidney Mitochondria
by Alexander Panov, Vladimir I. Mayorov and Sergey Dikalov
Int. J. Mol. Sci. 2022, 23(7), 4047; https://doi.org/10.3390/ijms23074047 - 06 Apr 2022
Cited by 11 | Viewed by 3617
Abstract
We present evidence that metabolic syndrome (MetS) represents the postreproductive stage of the human postembryonic ontogenesis. Accordingly, the genes governing this stage experience relatively weak evolutionary selection pressure, thus representing the metabolic phenotype of distant ancestors with β-oxidation of long-chain fatty acids (FAs) [...] Read more.
We present evidence that metabolic syndrome (MetS) represents the postreproductive stage of the human postembryonic ontogenesis. Accordingly, the genes governing this stage experience relatively weak evolutionary selection pressure, thus representing the metabolic phenotype of distant ancestors with β-oxidation of long-chain fatty acids (FAs) as the primary energy source. Mitochondria oxidize at high-rate FAs only when succinate, glutamate, or pyruvate are present. The heart and brain mitochondria work at a wide range of functional loads and possess an intrinsic inhibition of complex II to prevent oxidative stress at periods of low functional activity. Kidney mitochondria constantly work at a high rate and lack inhibition of complex II. We suggest that in people with MetS, oxidative stress is the central mechanism of the heart and brain pathologies. Oxidative stress is a secondary pathogenetic mechanism in the kidney, while the primary mechanisms are kidney hypoxia caused by persistent hyperglycemia and hypertension. Current evidence suggests that most of the nongenetic pathologies associated with MetS originate from the inconsistencies between the metabolic phenotype acquired after the transition to the postreproductive stage and excessive consumption of food rich in carbohydrates and a sedentary lifestyle. Full article
(This article belongs to the Special Issue Mitochondria: Aging, Metabolic Syndrome and Cardiovascular Diseases)
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16 pages, 691 KiB  
Review
The Role of Mitochondrial DNA Mutations in Cardiovascular Diseases
by Siarhei A. Dabravolski, Victoria A. Khotina, Vasily N. Sukhorukov, Vladislav A. Kalmykov, Liudmila M. Mikhaleva and Alexander N. Orekhov
Int. J. Mol. Sci. 2022, 23(2), 952; https://doi.org/10.3390/ijms23020952 - 16 Jan 2022
Cited by 19 | Viewed by 4115
Abstract
Cardiovascular diseases (CVD) are one of the leading causes of morbidity and mortality worldwide. mtDNA (mitochondrial DNA) mutations are known to participate in the development and progression of some CVD. Moreover, specific types of mitochondria-mediated CVD have been discovered, such as MIEH (maternally [...] Read more.
Cardiovascular diseases (CVD) are one of the leading causes of morbidity and mortality worldwide. mtDNA (mitochondrial DNA) mutations are known to participate in the development and progression of some CVD. Moreover, specific types of mitochondria-mediated CVD have been discovered, such as MIEH (maternally inherited essential hypertension) and maternally inherited CHD (coronary heart disease). Maternally inherited mitochondrial CVD is caused by certain mutations in the mtDNA, which encode structural mitochondrial proteins and mitochondrial tRNA. In this review, we focus on recently identified mtDNA mutations associated with CVD (coronary artery disease and hypertension). Additionally, new data suggest the role of mtDNA mutations in Brugada syndrome and ischemic stroke, which before were considered only as a result of mutations in nuclear genes. Moreover, we discuss the molecular mechanisms of mtDNA involvement in the development of the disease. Full article
(This article belongs to the Special Issue Mitochondria: Aging, Metabolic Syndrome and Cardiovascular Diseases)
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