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Metabolites
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Autophagy, Aging and Metabolism
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Autophagy, Aging and Metabolism

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Cell Metabolism".

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 23410

Special Issue Editors

Dr. Guillermo Mariño

E-Mail Website1 Website2
Guest Editor
1. Principality of Asturias Sanitary Research Institute (ISPA), Oviedo, Spain
2. Department of Functional Biology, University of Oviedo, Oviedo, Spain
Interests: autophagy; metabolism; animal models; aging; longevity
Dr. Álvaro F. Fernández

E-Mail
Guest Editor
1. Department of Functional Biology, University of Oviedo, Oviedo, Spain
2. Principality of Asturias Sanitary Research Institute (ISPA), Oviedo, Spain
Interests: autophagy; aging; animal models; metabolism; cell death
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Over the last several years, we have started to comprehend the molecular basis of aging. Given its intricate nature, the number of biological factors to be considered when obtaining insights into the aging process is overwhelmingly vast. However, despite the inherent complexity of aging, we have begun to understand that cellular metabolism is one of the key players in the process. In fact, metabolic modulation and rewiring are at the core of most of the currently known nutritional, genetic, and pharmacological manipulations able to extend longevity in laboratory model organisms, including mammals.

Among the great variety of metabolic processes, autophagy is probably one of the most interesting. Autophagy is an evolutionarily conserved catabolic pathway that assists eukaryotic cells when they need to counteract a wide variety of adverse conditions. Moreover, autophagy’s role as a housekeeping mechanism is essential for cell, tissue, and organism homeostasis. This Special Issue focuses on reviewing the connections among autophagy, metabolism, and aging. We therefore call for review and viewpoint manuscripts devoted to addressing various aspects of the intricate links between these three processes. These studies can be either focused on specific age-related pathologies or on the aging process itself. We also invite original manuscripts addressing new findings in the fields of autophagy, metabolism, and aging. Finally, we welcome studies covering how modulation of autophagy and other metabolic processes may influence longevity, from any specific point of view aimed at a better understanding the molecular basis of the aging process.

Dr. Guillermo Mariño
Dr. Álvaro F. Fernández
Guest Editors

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. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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.

Keywords

  • autophagy
  • metabolism
  • aging
  • longevity
  • calorie restriction
  • lifespan extension
  • healthspan

Published Papers (5 papers)

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Research

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18 pages, 2722 KiB  
Article
Metabolomic Profiles of Mouse Tissues Reveal an Interplay between Aging and Energy Metabolism
by Qishun Zhou, Jakob Kerbl-Knapp, Fangrong Zhang, Melanie Korbelius, Katharina Barbara Kuentzel, Nemanja Vujić, Alena Akhmetshina, Gerd Hörl, Margret Paar, Ernst Steyrer, Dagmar Kratky and Tobias Madl
Metabolites 2022, 12(1), 17; https://0-doi-org.brum.beds.ac.uk/10.3390/metabo12010017 - 26 Dec 2021
Cited by 9 | Viewed by 3922
Abstract
Energy metabolism, including alterations in energy intake and expenditure, is closely related to aging and longevity. Metabolomics studies have recently unraveled changes in metabolite composition in plasma and tissues during aging and have provided critical information to elucidate the molecular basis of the [...] Read more.
Energy metabolism, including alterations in energy intake and expenditure, is closely related to aging and longevity. Metabolomics studies have recently unraveled changes in metabolite composition in plasma and tissues during aging and have provided critical information to elucidate the molecular basis of the aging process. However, the metabolic changes in tissues responsible for food intake and lipid storage have remained unexplored. In this study, we aimed to investigate aging-related metabolic alterations in these tissues. To fill this gap, we employed NMR-based metabolomics in several tissues, including different parts of the intestine (duodenum, jejunum, ileum) and brown/white adipose tissues (BAT, WAT), of young (9–10 weeks) and old (96–104 weeks) wild-type (mixed genetic background of 129/J and C57BL/6) mice. We, further, included plasma and skeletal muscle of the same mice to verify previous results. Strikingly, we found that duodenum, jejunum, ileum, and WAT do not metabolically age. In contrast, plasma, skeletal muscle, and BAT show a strong metabolic aging phenotype. Overall, we provide first insights into the metabolic changes of tissues essential for nutrient uptake and lipid storage and have identified biomarkers for metabolites that could be further explored, to study the molecular mechanisms of aging. Full article
(This article belongs to the Special Issue Autophagy, Aging and Metabolism)
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15 pages, 1795 KiB  
Article
Stimulation of Toll-Like Receptor 3 Diminishes Intracellular Growth of Salmonella Typhimurium by Enhancing Autophagy in Murine Macrophages
by Hyo-Ji Lee, Sun-Hye Lee, Ji-Hui Jeon, Hyo-Jung Kim, Eui-Kwon Jeong, Min-Jeong Kim, Young Mee Jung and Yu-Jin Jung
Metabolites 2021, 11(9), 602; https://0-doi-org.brum.beds.ac.uk/10.3390/metabo11090602 - 04 Sep 2021
Cited by 1 | Viewed by 2130
Abstract
The Salmonella enterica serovar Typhimurium (S. Typhimurium) is a facultative Gram-negative bacterium that causes acute gastroenteritis and food poisoning. S. Typhimurium can survive within macrophages that are able to initiate the innate immune response after recognizing bacteria via various pattern-recognition receptors [...] Read more.
The Salmonella enterica serovar Typhimurium (S. Typhimurium) is a facultative Gram-negative bacterium that causes acute gastroenteritis and food poisoning. S. Typhimurium can survive within macrophages that are able to initiate the innate immune response after recognizing bacteria via various pattern-recognition receptors (PRRs), such as Toll-like receptors (TLRs). In this study, we investigated the effects and molecular mechanisms by which agonists of endosomal TLRs—especially TLR3—contribute to controlling S. Typhimurium infection in murine macrophages. Treatment with polyinosinic:polycytidylic acid (poly(I:C))—an agonist of TLR3—significantly suppressed intracellular bacterial growth by promoting intracellular ROS production in S. Typhimurium-infected cells. Pretreatment with diphenyleneiodonium (DPI)—an NADPH oxidase inhibitor—reduced phosphorylated MEK1/2 levels and restored intracellular bacterial growth in poly(I:C)-treated cells during S. Typhimurium infection. Nitric oxide (NO) production increased through the NF-κB-mediated signaling pathway in poly(I:C)-treated cells during S. Typhimurium infection. Intracellular microtubule-associated protein 1A/1B-light chain 3 (LC3) levels were increased in poly(I:C)-treated cells; however, they were decreased in cells pretreated with 3-methyladenine (3-MA)—a commonly used inhibitor of autophagy. These results suggest that poly(I:C) induces autophagy and enhances ROS production via MEK1/2-mediated signaling to suppress intracellular bacterial growth in S. Typhimurium-infected murine macrophages, and that a TLR3 agonist could be developed as an immune enhancer to protect against S. Typhimurium infection. Full article
(This article belongs to the Special Issue Autophagy, Aging and Metabolism)
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18 pages, 28597 KiB  
Article
Autophagy Deficiency by Atg4B Loss Leads to Metabolomic Alterations in Mice
by Gemma G. Martínez-García, Raúl F. Pérez, Álvaro F. Fernández, Sylvere Durand, Guido Kroemer and Guillermo Mariño
Metabolites 2021, 11(8), 481; https://0-doi-org.brum.beds.ac.uk/10.3390/metabo11080481 - 27 Jul 2021
Cited by 6 | Viewed by 2469
Abstract
Autophagy is an essential protective mechanism that allows mammalian cells to cope with a variety of stressors and contributes to maintaining cellular and tissue homeostasis. Due to these crucial roles and also to the fact that autophagy malfunction has been described in a [...] Read more.
Autophagy is an essential protective mechanism that allows mammalian cells to cope with a variety of stressors and contributes to maintaining cellular and tissue homeostasis. Due to these crucial roles and also to the fact that autophagy malfunction has been described in a wide range of pathologies, an increasing number of in vivo studies involving animal models targeting autophagy genes have been developed. In mammals, total autophagy inactivation is lethal, and constitutive knockout models lacking effectors of this route are not viable, which has hindered so far the analysis of the consequences of a systemic autophagy decline. Here, we take advantage of atg4b−/− mice, an autophagy-deficient model with only partial disruption of the process, to assess the effects of systemic reduction of autophagy on the metabolome. We describe for the first time the metabolic footprint of systemic autophagy decline, showing that impaired autophagy results in highly tissue-dependent alterations that are more accentuated in the skeletal muscle and plasma. These changes, which include changes in the levels of amino-acids, lipids, or nucleosides, sometimes resemble those that are frequently described in conditions like aging, obesity, or cardiac damage. We also discuss different hypotheses on how impaired autophagy may affect the metabolism of several tissues in mammals. Full article
(This article belongs to the Special Issue Autophagy, Aging and Metabolism)
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16 pages, 1781 KiB  
Article
Trehalose Reduces the Secreted Beta-Amyloid Levels in Primary Neurons Independently of Autophagy Induction
by Irene Benito-Cuesta, Lara Ordoñez-Gutierrez and Francisco Wandosell
Metabolites 2021, 11(7), 421; https://0-doi-org.brum.beds.ac.uk/10.3390/metabo11070421 - 26 Jun 2021
Cited by 6 | Viewed by 2479
Abstract
The disaccharide trehalose was described as possessing relevant neuroprotective properties as an mTORC1-independent inducer of autophagy, with the ability to protect cellular membranes and denaturation, resulting from desiccation, and preventing the cellular accumulation of protein aggregates. These properties make trehalose an interesting therapeutic [...] Read more.
The disaccharide trehalose was described as possessing relevant neuroprotective properties as an mTORC1-independent inducer of autophagy, with the ability to protect cellular membranes and denaturation, resulting from desiccation, and preventing the cellular accumulation of protein aggregates. These properties make trehalose an interesting therapeutic candidate against proteinopathies such as Alzheimer’s disease (AD), which is characterized by deposits of aggregated amyloid-beta (Aβ) and hyperphosphorylated tau. In this study, we observed that trehalose was able to induce autophagy in neurons only in the short-term, whereas long-term treatment with trehalose provoked a relevant anti-amyloidogenic effect in neurons from an AD mouse model that was not mediated by autophagy. Trehalose treatment reduced secreted Aβ levels in a manner unrelated to its intracellular accumulation or its elimination through endocytosis or enzymatic degradation. Moreover, the levels of Aβ precursor protein (APP) and beta-secretase (BACE1) remained unaltered, as well as the proper acidic condition of the endo-lysosome system. Instead, our results support that the neuroprotective effect of trehalose was mediated by a reduced colocalization of APP and BACE1 in the cell, and, therefore, a lower amyloidogenic processing of APP. This observation illustrates that the determination of the mechanism, or mechanisms, that associate APP and BACE is a relevant therapeutic target to investigate. Full article
(This article belongs to the Special Issue Autophagy, Aging and Metabolism)
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Review

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12 pages, 676 KiB  
Review
Selective Autophagy as a Potential Therapeutic Target in Age-Associated Pathologies
by Margarita-Elena Papandreou and Nektarios Tavernarakis
Metabolites 2021, 11(9), 588; https://0-doi-org.brum.beds.ac.uk/10.3390/metabo11090588 - 31 Aug 2021
Cited by 1 | Viewed by 11304
Abstract
Progressive accumulation of damaged cellular constituents contributes to age-related diseases. Autophagy is the main catabolic process, which recycles cellular material in a multitude of tissues and organs. Autophagy is activated upon nutrient deprivation, and oncogenic, heat or oxidative stress-induced stimuli to selectively degrade [...] Read more.
Progressive accumulation of damaged cellular constituents contributes to age-related diseases. Autophagy is the main catabolic process, which recycles cellular material in a multitude of tissues and organs. Autophagy is activated upon nutrient deprivation, and oncogenic, heat or oxidative stress-induced stimuli to selectively degrade cell constituents and compartments. Specificity and accuracy of the autophagic process is maintained via the precision of interaction of autophagy receptors or adaptors and substrates by the intricate, stepwise orchestration of specialized integrating stimuli. Polymorphisms in genes regulating selective autophagy have been linked to aging and age-associated disorders. The involvement of autophagy perturbations in aging and disease indicates that pharmacological agents balancing autophagic flux may be beneficial, in these contexts. Here, we introduce the modes and mechanisms of selective autophagy, and survey recent experimental evidence of dysfunctional autophagy triggering severe pathology. We further highlight identified pharmacological targets that hold potential for developing therapeutic interventions to alleviate cellular autophagic cargo burden and associated pathologies. Full article
(This article belongs to the Special Issue Autophagy, Aging and Metabolism)
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