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Cells
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Understanding Aging Mechanisms to Prevent Age-Related Diseases
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Understanding Aging Mechanisms to Prevent Age-Related Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Aging".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 7033

Special Issue Editors

Prof. Dr. Pierre Jouanny

E-Mail Website
Guest Editor
Team U1093 CAPS “Cognition, Action and Sensorimotor Plasticity”, Université de Bourgogne, 21000 Dijon, France
Interests: Alzheimer’s disease; frailty; ageing process; epidemiology; successful aging
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Sonia Hammami

E-Mail Website
Guest Editor
Lab-NAFS ‘Nutritio—Functional Food & Vascular Health’, Faculty of Medicine, LR12ES05, University Monastir, Monastir 5000, Tunisia
Interests: aging; geriatrics; frailty; sarcopenia; Alzheimer’s disease; nutrition
Special Issues, Collections and Topics in MDPI journals
Dr. Gérard Lizard

E-Mail Website
Guest Editor
Team "Biochemistry of the Peroxisome, Inflammation and Lipid Metabolism", Université de Bourgogne Franche-Comté, 21000 Dijon, France
Interests: lipids; oxysterols; fatty acids; polyphenols; oils; oxidation; inflammation; mitochondria; peroxisomes; lysosomes; apoptosis; autophagy; natural products; synthethic molecules; biomarkers; neurodegeneration; neurodegenerative diseases; aging; age-related diseases; nanoparticles; targeted therapy
Special Issues, Collections and Topics in MDPI journals
Dr. Anne Vejux

E-Mail Website
Guest Editor
Team “Biochemistry of the Peroxisome, Inflammation and Lipid Metabolism”, Université de Bourgogne, 21000 Dijon, France
Interests: oxysterols; very-long-chain fatty acids; lipid metabolism; diet, peroxisomes; biotherapies; inflammation; cancer; cell cycle and apoptosis; autophagy; biological membranes; oxidative damage; biomarkers; neurodegenerative diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

During recent decades, the percentage of people over 65, as well as the lifespan, has increased considerably and is expected to increase further in the coming years. Aging in good health has therefore become a societal and economic issue. Therefore, understanding the mechanisms of aging and preventing it by opposing the onset of age-related diseases is a public health issue. In this context, it is important to identify the genetic and epigenetic factors that can influence aging and to determine the associated mechanisms. It is now crucial to determine strategies to slow aging in order to oppose the onset of age-related diseases. Identifying predictive biomarkers of age-related diseases is a major challenge, as is the discovery of molecules that can oppose aging and the occurrence of associated diseases. This Special Issue of Cells entitled 'Understanding Aging Mechanisms to Prevent Age-Related Diseases' aims to bring together relevant research works dealing with cellular and molecular, pharmacological and nutritional aspects of aging and age-related diseases.

Prof. Dr. Pierre Jouanny
Prof. Dr. Sonia Hammami
Dr. Gérard Lizard
Dr. Anne Vejux
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. Cells is an international peer-reviewed open access semimonthly 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.

Published Papers (3 papers)

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Research

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20 pages, 15361 KiB  
Article
GABA Prevents Age-Related Sarcopenic Obesity in Mice with High-Fat-Diet-Induced Obesity
by Heegu Jin, Hyun-Ji Oh and Boo-Yong Lee
Cells 2023, 12(17), 2146; https://doi.org/10.3390/cells12172146 - 25 Aug 2023
Cited by 2 | Viewed by 1902
Abstract
Sarcopenic obesity is characterized by concurrent obesity and muscle wasting (sarcopenia) and is common in the elderly. Sarcopenic obesity has steadily increased as the aging population has grown and is an increasing public health burden. Both obesity and sarcopenia independently increase health risks [...] Read more.
Sarcopenic obesity is characterized by concurrent obesity and muscle wasting (sarcopenia) and is common in the elderly. Sarcopenic obesity has steadily increased as the aging population has grown and is an increasing public health burden. Both obesity and sarcopenia independently increase health risks of the elderly, but sarcopenic obesity has a greater effect on metabolic disease than either obesity or sarcopenia alone. The metabolic mechanisms of obesity and sarcopenia are strongly interconnected, and obesity and sarcopenia form a vicious cycle, with each pathology exacerbating the other. The pathogenesis of sarcopenic obesity is more complex than either disease alone and remains incompletely understood, underscoring the significant unmet clinical need for effective sarcopenic obesity treatments. We aimed to determine the efficacy and underlying regulatory mechanisms of Gamma-aminobutyric acid (GABA) in sarcopenic obesity in high-fat-diet-fed obese aged mice and alterations in related mechanisms to determine the potential of GABA as a therapeutic modality for sarcopenic obesity. In this study, we used young (3 months) and aged (20 months) mice to evaluate age-related sarcopenic obesity. The daily administration of GABA for 8 weeks resulted in decreased fat mass and increased muscle mass and strength in aged mice. GABA also enhanced energy expenditure in both adipose tissue and skeletal muscle. In addition, GABA promoted muscle synthesis and decreased muscle degradation by activating the phosphatidylinositol-3-kinase (PI3K)/Akt pathway. These findings demonstrate that GABA has potential uses in preventing age-related sarcopenic obesity and related metabolic diseases. Full article
(This article belongs to the Special Issue Understanding Aging Mechanisms to Prevent Age-Related Diseases)
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Review

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30 pages, 3758 KiB  
Review
Unraveling Histone Loss in Aging and Senescence
by Sushil Kumar Dubey, Rashmi Dubey and Mark Ellsworth Kleinman
Cells 2024, 13(4), 320; https://doi.org/10.3390/cells13040320 - 09 Feb 2024
Viewed by 1724
Abstract
As the global population experiences a notable surge in aging demographics, the need to understand the intricate molecular pathways exacerbated by age-related stresses, including epigenetic dysregulation, becomes a priority. Epigenetic mechanisms play a critical role in driving age-related diseases through altered gene expression, [...] Read more.
As the global population experiences a notable surge in aging demographics, the need to understand the intricate molecular pathways exacerbated by age-related stresses, including epigenetic dysregulation, becomes a priority. Epigenetic mechanisms play a critical role in driving age-related diseases through altered gene expression, genomic instability, and irregular chromatin remodeling. In this review, we focus on histones, a central component of the epigenome, and consolidate the key findings of histone loss and genome-wide redistribution as fundamental processes contributing to aging and senescence. The review provides insights into novel histone expression profiles, nucleosome occupancy, disruptions in higher-order chromatin architecture, and the emergence of noncanonical histone variants in the aging cellular landscape. Furthermore, we explore the current state of our understanding of the molecular mechanisms of histone deficiency in aging cells. Specific emphasis is placed on highlighting histone degradation pathways in the cell and studies that have explored potential strategies to mitigate histone loss or restore histone levels in aging cells. Finally, in addressing future perspectives, the insights gained from this review hold profound implications for advancing strategies that actively intervene in modulating histone expression profiles in the context of cellular aging and identifying potential therapeutic targets for alleviating a multitude of age-related diseases. Full article
(This article belongs to the Special Issue Understanding Aging Mechanisms to Prevent Age-Related Diseases)
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23 pages, 1157 KiB  
Review
Reappraisal of the Concept of Accelerated Aging in Neurodegeneration and Beyond
by Yauhen Statsenko, Nik V. Kuznetsov, Daria Morozova, Katsiaryna Liaonchyk, Gillian Lylian Simiyu, Darya Smetanina, Aidar Kashapov, Sarah Meribout, Klaus Neidl-Van Gorkom, Rifat Hamoudi, Fatima Ismail, Suraiya Anjum Ansari, Bright Starling Emerald and Milos Ljubisavljevic
Cells 2023, 12(20), 2451; https://doi.org/10.3390/cells12202451 - 14 Oct 2023
Viewed by 2360
Abstract
Background: Genetic and epigenetic changes, oxidative stress and inflammation influence the rate of aging, which diseases, lifestyle and environmental factors can further accelerate. In accelerated aging (AA), the biological age exceeds the chronological age. Objective: The objective of this study is to reappraise [...] Read more.
Background: Genetic and epigenetic changes, oxidative stress and inflammation influence the rate of aging, which diseases, lifestyle and environmental factors can further accelerate. In accelerated aging (AA), the biological age exceeds the chronological age. Objective: The objective of this study is to reappraise the AA concept critically, considering its weaknesses and limitations. Methods: We reviewed more than 300 recent articles dealing with the physiology of brain aging and neurodegeneration pathophysiology. Results: (1) Application of the AA concept to individual organs outside the brain is challenging as organs of different systems age at different rates. (2) There is a need to consider the deceleration of aging due to the potential use of the individual structure–functional reserves. The latter can be restored by pharmacological and/or cognitive therapy, environment, etc. (3) The AA concept lacks both standardised terminology and methodology. (4) Changes in specific molecular biomarkers (MBM) reflect aging-related processes; however, numerous MBM candidates should be validated to consolidate the AA theory. (5) The exact nature of many potential causal factors, biological outcomes and interactions between the former and the latter remain largely unclear. Conclusions: Although AA is commonly recognised as a perspective theory, it still suffers from a number of gaps and limitations that assume the necessity for an updated AA concept. Full article
(This article belongs to the Special Issue Understanding Aging Mechanisms to Prevent Age-Related Diseases)
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