Role of Mitochondria in Environmentally and Dietary Modulated Age-Associated Diseases

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (15 November 2021) | Viewed by 35464

Special Issue Editors


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Guest Editor
Mitochondria in Environmentally Induced Neuronal Aging and Pathologies, Institute of Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University of Duesseldorf and the Leibniz Research Institute for Environmental Medicine, Dusseldorf, Germany
Interests: mitochondria; aging; neuropathologies; C. elegans

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Guest Editor
1. Cardiovascular Degeneration, Haendeler Group, Clinical Chemistry and Laboratory Diagnostics, Medical Faculty, University Hospital, Heinrich-Heine University Duesseldorf, 40225 Duesseldorf, Germany
2. Cardiovascular Research Institute Düsseldorf (CARID), Medical Faculty, University Hospital, Heinrich-Heine University Duesseldorf, 40225 Duesseldorf, Germany
Interests: cardiovascular diseases; redox regulation; mitochondria; aging

Special Issue Information

Dear Colleagues,

Aging is the most important risk factor for the development of a large number of disorders. Genetic factors, but more prominent environmental factors including diet concurrently shape human health and aging. On the one hand external insults such as pesticides or radiations as well as products of endogenous metabolism, may negatively impact on disease development and progression and may accelerate the aging process. On the other hand, several food components or supplements, have been described or proposed to promote health and longevity. Due to the wide range of external stimuli and insults, numerous molecular mechanisms are involved in the modulation of cell and organim homeostasis. Mitochondria are key players of energy metabolism, but in our days are also appreciated as signaling organelles and in such a way certainly represent central hubs in cellular responses to environmental factors.

The primary focus of this special issue will be to highlight our current knowledge on the important role of mitochondria in environmentally including dietary modulated aging and associated diseases. Moreover, relevant manuscripts will primarily investigate novel underlying molecular mechanisms of environmental factors in modulating mitochondrial or mitochondria-related intracellular functions with direct consequences on aging and associated diseases, along with possible targeted preventive or therapeutic strategies.

Dr. Natascia Ventura
Prof. Dr. Judith Haendeler
Guest Editors

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Keywords

  • mitochondria
  • environmental factors including dietary components
  • aging
  • age-associated diseases
  • metabolism
  • prevention and therapies

Published Papers (6 papers)

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Editorial

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3 pages, 193 KiB  
Editorial
Role of Mitochondria in Environmentally and Dietary Modulated Age-Associated Diseases
by Natascia Ventura and Judith Haendeler
Cells 2023, 12(3), 404; https://doi.org/10.3390/cells12030404 - 25 Jan 2023
Viewed by 1071
Abstract
Aging is an intricate and unavoidable phenomenon characterized by progressive accumulation of damage to cellular structural components with consequent decline in physiological functions and development of different pathological conditions, which lead to increase in frailty and mortality risk and bring a huge economic [...] Read more.
Aging is an intricate and unavoidable phenomenon characterized by progressive accumulation of damage to cellular structural components with consequent decline in physiological functions and development of different pathological conditions, which lead to increase in frailty and mortality risk and bring a huge economic burden in our society [...] Full article

Research

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19 pages, 3773 KiB  
Article
High-Content C. elegans Screen Identifies Natural Compounds Impacting Mitochondria-Lipid Homeostasis and Promoting Healthspan
by Silvia Maglioni, Nayna Arsalan, Anna Hamacher, Shiwa Afshar, Alfonso Schiavi, Mathias Beller and Natascia Ventura
Cells 2022, 11(1), 100; https://doi.org/10.3390/cells11010100 - 29 Dec 2021
Cited by 9 | Viewed by 3219
Abstract
The aging process is concurrently shaped by genetic and extrinsic factors. In this work, we screened a small library of natural compounds, many of marine origin, to identify novel possible anti-aging interventions in Caenorhabditis elegans, a powerful model organism for aging studies. [...] Read more.
The aging process is concurrently shaped by genetic and extrinsic factors. In this work, we screened a small library of natural compounds, many of marine origin, to identify novel possible anti-aging interventions in Caenorhabditis elegans, a powerful model organism for aging studies. To this aim, we exploited a high-content microscopy platform to search for interventions able to induce phenotypes associated with mild mitochondrial stress, which is known to promote animal’s health- and lifespan. Worms were initially exposed to three different concentrations of the drugs in liquid culture, in search of those affecting animal size and expression of mitochondrial stress response genes. This was followed by a validation step with nine compounds on solid media to refine compounds concentration, which led to the identification of four compounds (namely isobavachalcone, manzamine A, kahalalide F and lutein) consistently affecting development, fertility, size and lipid content of the nematodes. Treatment of Drosophila cells with the four hits confirmed their effects on mitochondria activity and lipid content. Out of these four, two were specifically chosen for analysis of age-related parameters, kahalalide F and lutein, which conferred increased resistance to heat and oxidative stress and extended animals’ healthspan. We also found that, out of different mitochondrial stress response genes, only the C. elegans ortholog of the synaptic regulatory proteins neuroligins, nlg-1, was consistently induced by the two compounds and mediated lutein healthspan effects. Full article
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Review

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24 pages, 2374 KiB  
Review
Protective Effects of Curcumin in Cardiovascular Diseases—Impact on Oxidative Stress and Mitochondria
by Fiona Frederike Cox, Angelina Misiou, Annika Vierkant, Niloofar Ale-Agha, Maria Grandoch, Judith Haendeler and Joachim Altschmied
Cells 2022, 11(3), 342; https://doi.org/10.3390/cells11030342 - 20 Jan 2022
Cited by 53 | Viewed by 8304
Abstract
Cardiovascular diseases (CVDs) contribute to a large part of worldwide mortality. Similarly, two of the major risk factors for these diseases, aging and obesity, are also global problems. Aging, the gradual decline of body functions, is non-modifiable. Obesity, a modifiable risk factor for [...] Read more.
Cardiovascular diseases (CVDs) contribute to a large part of worldwide mortality. Similarly, two of the major risk factors for these diseases, aging and obesity, are also global problems. Aging, the gradual decline of body functions, is non-modifiable. Obesity, a modifiable risk factor for CVDs, also predisposes to type 2 diabetes mellitus (T2DM). Moreover, it affects not only the vasculature and the heart but also specific fat depots, which themselves have a major impact on the development and progression of CVDs. Common denominators of aging, obesity, and T2DM include oxidative stress, mitochondrial dysfunction, metabolic abnormalities such as altered lipid profiles and glucose metabolism, and inflammation. Several plant substances such as curcumin, the major active compound in turmeric root, have been used for a long time in traditional medicine and for the treatment of CVDs. Newer mechanistic, animal, and human studies provide evidence that curcumin has pleiotropic effects and attenuates numerous parameters which contribute to an increased risk for CVDs in aging as well as in obesity. Thus, curcumin as a nutraceutical could hold promise in the prevention of CVDs, but more standardized clinical trials are required to fully unravel its potential. Full article
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26 pages, 1798 KiB  
Review
One-Carbon Metabolism: Pulling the Strings behind Aging and Neurodegeneration
by Eirini Lionaki, Christina Ploumi and Nektarios Tavernarakis
Cells 2022, 11(2), 214; https://doi.org/10.3390/cells11020214 - 9 Jan 2022
Cited by 29 | Viewed by 11414
Abstract
One-carbon metabolism (OCM) is a network of biochemical reactions delivering one-carbon units to various biosynthetic pathways. The folate cycle and methionine cycle are the two key modules of this network that regulate purine and thymidine synthesis, amino acid homeostasis, and epigenetic mechanisms. Intersection [...] Read more.
One-carbon metabolism (OCM) is a network of biochemical reactions delivering one-carbon units to various biosynthetic pathways. The folate cycle and methionine cycle are the two key modules of this network that regulate purine and thymidine synthesis, amino acid homeostasis, and epigenetic mechanisms. Intersection with the transsulfuration pathway supports glutathione production and regulation of the cellular redox state. Dietary intake of micronutrients, such as folates and amino acids, directly contributes to OCM, thereby adapting the cellular metabolic state to environmental inputs. The contribution of OCM to cellular proliferation during development and in adult proliferative tissues is well established. Nevertheless, accumulating evidence reveals the pivotal role of OCM in cellular homeostasis of non-proliferative tissues and in coordination of signaling cascades that regulate energy homeostasis and longevity. In this review, we summarize the current knowledge on OCM and related pathways and discuss how this metabolic network may impact longevity and neurodegeneration across species. Full article
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16 pages, 1414 KiB  
Review
Mitochondrial Dysfunction as a Hallmark of Environmental Injury
by Carolina Duarte-Hospital, Arnaud Tête, François Brial, Louise Benoit, Meriem Koual, Céline Tomkiewicz, Min Ji Kim, Etienne B. Blanc, Xavier Coumoul and Sylvie Bortoli
Cells 2022, 11(1), 110; https://doi.org/10.3390/cells11010110 - 30 Dec 2021
Cited by 25 | Viewed by 4532
Abstract
Environmental factors including diet, sedentary lifestyle and exposure to pollutants largely influence human health throughout life. Cellular and molecular events triggered by an exposure to environmental pollutants are extremely variable and depend on the age, the chronicity and the doses of exposure. Only [...] Read more.
Environmental factors including diet, sedentary lifestyle and exposure to pollutants largely influence human health throughout life. Cellular and molecular events triggered by an exposure to environmental pollutants are extremely variable and depend on the age, the chronicity and the doses of exposure. Only a fraction of all relevant mechanisms involved in the onset and progression of pathologies in response to toxicants has probably been identified. Mitochondria are central hubs of metabolic and cell signaling responsible for a large variety of biochemical processes, including oxidative stress, metabolite production, energy transduction, hormone synthesis, and apoptosis. Growing evidence highlights mitochondrial dysfunction as a major hallmark of environmental insults. Here, we present mitochondria as crucial organelles for healthy metabolic homeostasis and whose dysfunction induces critical adverse effects. Then, we review the multiple mechanisms of action of pollutants causing mitochondrial toxicity in link with chronic diseases. We propose the Aryl hydrocarbon Receptor (AhR) as a model of “exposome receptor”, whose activation by environmental pollutants leads to various toxic events through mitochondrial dysfunction. Finally, we provide some remarks related to mitotoxicity and risk assessment. Full article
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22 pages, 2927 KiB  
Review
Role of Mitochondrial Protein Import in Age-Related Neurodegenerative and Cardiovascular Diseases
by Andrey Bogorodskiy, Ivan Okhrimenko, Dmitrii Burkatovskii, Philipp Jakobs, Ivan Maslov, Valentin Gordeliy, Norbert A. Dencher, Thomas Gensch, Wolfgang Voos, Joachim Altschmied, Judith Haendeler and Valentin Borshchevskiy
Cells 2021, 10(12), 3528; https://doi.org/10.3390/cells10123528 - 14 Dec 2021
Cited by 6 | Viewed by 5861
Abstract
Mitochondria play a critical role in providing energy, maintaining cellular metabolism, and regulating cell survival and death. To carry out these crucial functions, mitochondria employ more than 1500 proteins, distributed between two membranes and two aqueous compartments. An extensive network of dedicated proteins [...] Read more.
Mitochondria play a critical role in providing energy, maintaining cellular metabolism, and regulating cell survival and death. To carry out these crucial functions, mitochondria employ more than 1500 proteins, distributed between two membranes and two aqueous compartments. An extensive network of dedicated proteins is engaged in importing and sorting these nuclear-encoded proteins into their designated mitochondrial compartments. Defects in this fundamental system are related to a variety of pathologies, particularly engaging the most energy-demanding tissues. In this review, we summarize the state-of-the-art knowledge about the mitochondrial protein import machinery and describe the known interrelation of its failure with age-related neurodegenerative and cardiovascular diseases. Full article
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