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Immunometabolic Disorders in Aging and Disease
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Immunometabolic Disorders in Aging and Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 5789

Special Issue Editors

Dr. Yury Ladilov

E-Mail Website
Guest Editor
Department of Cardiovascular Surgery, Heart Center Brandenburg, Brandenburg Medical School, 16321 Bernau, Germany
Interests: cAMP; AMPK; sirtuins; mitochondria; autophagy; heart failure; aging
Special Issues, Collections and Topics in MDPI journals
Dr. Maria Luisa Barcena

E-Mail Website
Guest Editor
Department of Geriatrics and Medical Gerontology, Charité, 12203 Berlin, Germany
Interests: cardiac aging; inflammaging; cardiac inflammation; mitochondrial function; cellular senescence; immunosenescence; immunometabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Immunometabolism (the crosstalk between the immune system and metabolism) regulates tissue homeostasis and several metabolic functions, and plays a crucial role in the development of chronic metabolic inflammation (metainflammation). Furthermore, the expression of pro- and anti-inflammatory cytokines and their effects appear to be profoundly affected by the systemic and immune cell metabolism. It is well documented that bioenergetic shifts modulate immune cell function. This is particularly obvious from the aging-related shift in cell metabolism from an anti-inflammatory to a pro-inflammatory phenotype.

Several studies have emphasized the importance of metabolic sensors, such as mTOR, AMP-activated protein kinase (AMPK), and sirtuins in inflammation, mitochondrial metabolism and immunometabolic pathways. Aging-related alterations in the activity or expression of these sensors, disturbed autophagy or compromised mitochondrial homeostasis may lead to numerous immunometabolic pathologies and diseases, such as insulin resistance, diabetes, metabolic syndrome and cardiovascular diseases. Therefore, understanding the mechanisms involved in the regulation and dysregulation of immunometabolic pathways may provide a basis for combating diseases and aging-associated dysfunctions. 

Authors are invited to submit manuscripts in all areas of current immunometabolism research, focusing either on basic or translational aspects, particularly related to aging and diseases. Studies addressing age-related changes in AMPK, sirtuins or mTOR pathways are explicitly encouraged. The Special Issue welcomes up-to-date hypotheses, reviews, research articles and short communications. Clinical studies combined with molecular research, if relevant, as well as computational modeling, are also welcome.

Dr. Yury Ladilov
Dr. Maria Luisa Barcena
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. 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.

Keywords

  • aging
  • immunometabolism
  • immunoaging
  • metainflammation
  • AMPK
  • mTOR
  • sirtuins
  • age-related chronic diseases
  • inflammation
  • longevity
  • mitophagy
  • autophagy
  • mitochondrial function
  • exercise
  • fasting
  • microbiome

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Published Papers (3 papers)

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Research

24 pages, 8623 KiB  
Article
Loss of Mitochondrial Tusc2/Fus1 Triggers a Brain Pro-Inflammatory Microenvironment and Early Spatial Memory Impairment
by Tonie Farris, Salvador González-Ochoa, Muna Mohammed, Harshana Rajakaruna, Jane Tonello, Thanigaivelan Kanagasabai, Olga Korolkova, Akiko Shimamoto, Alla Ivanova and Anil Shanker
Int. J. Mol. Sci. 2024, 25(13), 7406; https://doi.org/10.3390/ijms25137406 - 5 Jul 2024
Viewed by 1689
Abstract
Brain pathological changes impair cognition early in disease etiology. There is an urgent need to understand aging-linked mechanisms of early memory loss to develop therapeutic strategies and prevent the development of cognitive impairment. Tusc2 is a mitochondrial-resident protein regulating Ca2+ fluxes to [...] Read more.
Brain pathological changes impair cognition early in disease etiology. There is an urgent need to understand aging-linked mechanisms of early memory loss to develop therapeutic strategies and prevent the development of cognitive impairment. Tusc2 is a mitochondrial-resident protein regulating Ca2+ fluxes to and from mitochondria impacting overall health. We previously reported that Tusc2−/− female mice develop chronic inflammation and age prematurely, causing age- and sex-dependent spatial memory deficits at 5 months old. Therefore, we investigated Tusc2-dependent mechanisms of memory impairment in 4-month-old mice, comparing changes in resident and brain-infiltrating immune cells. Interestingly, Tusc2−/− female mice demonstrated a pro-inflammatory increase in astrocytes, expression of IFN-γ in CD4+ T cells and Granzyme-B in CD8+T cells. We also found fewer FOXP3+ T-regulatory cells and Ly49G+ NK and Ly49G+ NKT cells in female Tusc2−/− brains, suggesting a dampened anti-inflammatory response. Moreover, Tusc2−/− hippocampi exhibited Tusc2- and sex-specific protein changes associated with brain plasticity, including mTOR activation, and Calbindin and CamKII dysregulation affecting intracellular Ca2+ dynamics. Overall, the data suggest that dysregulation of Ca2+-dependent processes and a heightened pro-inflammatory brain microenvironment in Tusc2−/− mice could underlie cognitive impairment. Thus, strategies to modulate the mitochondrial Tusc2- and Ca2+- signaling pathways in the brain should be explored to improve cognitive health. Full article
(This article belongs to the Special Issue Immunometabolic Disorders in Aging and Disease)
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20 pages, 16892 KiB  
Article
Age-Dependent Inflammatory Microenvironment Mediates Alveolar Regeneration
by Rui Quan, Chenhong Shi, Bing Fang, Yanan Sun, Taiqi Qu, Xifan Wang, Ran Wang, Yiran Zhang, Fazheng Ren and Yixuan Li
Int. J. Mol. Sci. 2024, 25(6), 3476; https://doi.org/10.3390/ijms25063476 - 20 Mar 2024
Cited by 1 | Viewed by 1404
Abstract
Lung aging triggers the onset of various chronic lung diseases, with alveolar repair being a key focus for alleviating pulmonary conditions. The regeneration of epithelial structures, particularly the differentiation from type II alveolar epithelial (AT2) cells to type I alveolar epithelial (AT1) cells, [...] Read more.
Lung aging triggers the onset of various chronic lung diseases, with alveolar repair being a key focus for alleviating pulmonary conditions. The regeneration of epithelial structures, particularly the differentiation from type II alveolar epithelial (AT2) cells to type I alveolar epithelial (AT1) cells, serves as a prominent indicator of alveolar repair. Nonetheless, the precise role of aging in impeding alveolar regeneration and its underlying mechanism remain to be fully elucidated. Our study employed histological methods to examine lung aging effects on structural integrity and pathology. Lung aging led to alveolar collapse, disrupted epithelial structures, and inflammation. Additionally, a relative quantification analysis revealed age-related decline in AT1 and AT2 cells, along with reduced proliferation and differentiation capacities of AT2 cells. To elucidate the mechanisms underlying AT2 cell functional decline, we employed transcriptomic techniques and revealed a correlation between inflammatory factors and genes regulating proliferation and differentiation. Furthermore, a D-galactose-induced senescence model in A549 cells corroborated our omics experiments and confirmed inflammation-induced cell cycle arrest and a >30% reduction in proliferation/differentiation. Physiological aging-induced chronic inflammation impairs AT2 cell functions, hindering tissue repair and promoting lung disease progression. This study offers novel insights into chronic inflammation’s impact on stem cell-mediated alveolar regeneration. Full article
(This article belongs to the Special Issue Immunometabolic Disorders in Aging and Disease)
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15 pages, 2530 KiB  
Article
Metabolomic Signatures of Alzheimer’s Disease Indicate Brain Region-Specific Neurodegenerative Progression
by Mirela Ambeskovic, Giselle Hopkins, Tanzi Hoover, Jeffrey T. Joseph, Tony Montina and Gerlinde A. S. Metz
Int. J. Mol. Sci. 2023, 24(19), 14769; https://doi.org/10.3390/ijms241914769 - 30 Sep 2023
Cited by 5 | Viewed by 2123
Abstract
Pathological mechanisms contributing to Alzheimer’s disease (AD) are still elusive. Here, we identified the metabolic signatures of AD in human post-mortem brains. Using 1H NMR spectroscopy and an untargeted metabolomics approach, we identified (1) metabolomic profiles of AD and age-matched healthy subjects [...] Read more.
Pathological mechanisms contributing to Alzheimer’s disease (AD) are still elusive. Here, we identified the metabolic signatures of AD in human post-mortem brains. Using 1H NMR spectroscopy and an untargeted metabolomics approach, we identified (1) metabolomic profiles of AD and age-matched healthy subjects in post-mortem brain tissue, and (2) region-common and region-unique metabolome alterations and biochemical pathways across eight brain regions revealed that BA9 was the most affected. Phenylalanine and phosphorylcholine were mainly downregulated, suggesting altered neurotransmitter synthesis. N-acetylaspartate and GABA were upregulated in most regions, suggesting higher inhibitory activity in neural circuits. Other region-common metabolic pathways indicated impaired mitochondrial function and energy metabolism, while region-unique pathways indicated oxidative stress and altered immune responses. Importantly, AD caused metabolic changes in brain regions with less well-documented pathological alterations that suggest degenerative progression. The findings provide a new understanding of the biochemical mechanisms of AD and guide biomarker discovery for personalized risk prediction and diagnosis. Full article
(This article belongs to the Special Issue Immunometabolic Disorders in Aging and Disease)
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