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Molecular Mechanisms of the Aging Process
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Molecular Mechanisms of the Aging Process

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

Deadline for manuscript submissions: 20 June 2024 | Viewed by 5067

Special Issue Editors

Dr. Giuseppe Coppotelli

E-Mail Website
Guest Editor
George & Anne Ryan Institute for Neuroscience, College of Pharmacy, University of Rhode Island, Kingston, RI, USA
Interests: protein homeostasis; mitochondrial dysfunction; inflammation; models for ageing and age-related diseases and treatment strategies
Special Issues, Collections and Topics in MDPI journals
Dr. Jaime M. Ross

E-Mail Website
Guest Editor
1. George & Anne Ryan Institute for Neuroscience, College of Pharmacy, University of Rhode Island, Kingston, RI, USA
2. Department of Neuroscience, BioMedicum, Karolinska Institutet, Stockholm, Sweden
Interests: mitochondrial dysfunction; metabolism; epigenetics; development; brain plasticity; models for ageing and neurodegenerative diseases and possible treatments
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The past ten years have seen an explosion of research regarding the molecular mechanisms of the aging process, including the demonstration of an epigenetic clock that could be used to track aging and pioneering work on the use of the Yamanaka factors to reverse the overall process.

Genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, disabled macroautophagy, deregulated nutrient-sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication, chronic inflammation, and dysbiosis are the new revised hallmarks of aging implicated not only in the aging process but also in numerous diseases, many of which are age-related, including cancers, metabolic diseases and diabetes, inflammatory conditions, neuropathy, stroke, and neurodegenerative diseases, such as Alzheimer’s, Parkinson’s, and Huntington’s disease as well as amyotrophic lateral sclerosis. The challenge of the aging field is now to disentangle the interconnectedness of such hallmarks to determine their contributions to the overall aging process to be able to design new therapies that could ameliorate or slow down aging in humans. Lifestyle factors, such as calorie restriction and exercise, as well as small molecules, have shown increasing promise as possible treatments to improve aging and age-related diseases.

Join us as we explore advancements made in the vast field of aging research. This Special Issue calls for original research, mini and full reviews, and perspectives that address the progress and current standing of molecular mechanisms of the aging process in the following topics:

  • Aging;
  • Dementias and neurodegenerative diseases;
  • Treatments to counteract the aging process;
  • Protein homeostasis and mitochondrial quality control;
  • Chronic inflammation and inflammatory diseases;
  • Senescence and senolytics;
  • Oxidative stress;
  • Metabolic disorders and diabetes;
  • Reprogramming/regeneration;
  • Cancers;
  • Epigenetics.

Dr. Giuseppe Coppotelli
Dr. Jaime M. Ross
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.

Published Papers (4 papers)

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Research

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15 pages, 1063 KiB  
Article
Predictive Models of Life Span in Old Female Mice Based on Immune, Redox, and Behavioral Parameters
by Judith Félix, Irene Martínez de Toda, Estefanía Díaz-Del Cerro, Iris Sánchez-Del Pozo and Mónica De la Fuente
Int. J. Mol. Sci. 2024, 25(8), 4203; https://doi.org/10.3390/ijms25084203 - 10 Apr 2024
Viewed by 315
Abstract
The development of mathematical models capable of predicting the lifespan of animals is growing. However, there are no studies that compare the predictive power of different sets of parameters depending on the age of the animals. The aim of the present study is [...] Read more.
The development of mathematical models capable of predicting the lifespan of animals is growing. However, there are no studies that compare the predictive power of different sets of parameters depending on the age of the animals. The aim of the present study is to test whether mathematical models for life span prediction developed in adult female mice based on immune, redox, and behavioral parameters can predict life span in old animals and to develop new models in old mice. For this purpose, 29 variables, including parameters of immune function, redox state, and behavioral ones, were evaluated in old female Swiss mice (80 ± 4 weeks). Life span was registered when they died naturally. Firstly, we observed that the models developed in adults were not able to accurately predict the life span of old mice. Therefore, the immunity (adjusted R2 = 73.6%), redox (adjusted R2 = 46.5%), immunity-redox (adjusted R2 = 96.4%), and behavioral (adjusted R2 = 67.9%) models were developed in old age. Finally, the models were validated in another batch of mice. The developed models in old mice show certain similarities to those in adults but include different immune, redox, and behavioral markers, which highlights the importance of age in the prediction of life span. Full article
(This article belongs to the Special Issue Molecular Mechanisms of the Aging Process)
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18 pages, 4423 KiB  
Article
High-Dose Fenofibrate Stimulates Multiple Cellular Stress Pathways in the Kidney of Old Rats
by Agata Wrońska, Jacek Kieżun and Zbigniew Kmieć
Int. J. Mol. Sci. 2024, 25(5), 3038; https://doi.org/10.3390/ijms25053038 - 06 Mar 2024
Viewed by 532
Abstract
We investigated the age-related effects of the lipid-lowering drug fenofibrate on renal stress-associated effectors. Young and old rats were fed standard chow with 0.1% or 0.5% fenofibrate. The kidney cortex tissue structure showed typical aging-related changes. In old rats, 0.1% fenofibrate reduced the [...] Read more.
We investigated the age-related effects of the lipid-lowering drug fenofibrate on renal stress-associated effectors. Young and old rats were fed standard chow with 0.1% or 0.5% fenofibrate. The kidney cortex tissue structure showed typical aging-related changes. In old rats, 0.1% fenofibrate reduced the thickening of basement membranes, but 0.5% fenofibrate exacerbated interstitial fibrosis. The PCR array for stress and toxicity-related targets showed that 0.1% fenofibrate mildly downregulated, whereas 0.5% upregulated multiple genes. In young rats, 0.1% fenofibrate increased some antioxidant genes’ expression and decreased the immunoreactivity of oxidative stress marker 4-HNE. However, the activation of cellular antioxidant defenses was impaired in old rats. Fenofibrate modulated the expression of factors involved in hypoxia and osmotic stress signaling similarly in both age groups. Inflammatory response genes were variably modulated in the young rats, whereas old animals presented elevated expression of proinflammatory genes and TNFα immunoreactivity after 0.5% fenofibrate. In old rats, 0.1% fenofibrate more prominently than in young animals induced phospho-AMPK and PGC1α levels, and upregulated fatty acid oxidation genes. Our results show divergent effects of fenofibrate in young and old rat kidneys. The activation of multiple stress-associated effectors by high-dose fenofibrate in the aged kidney warrants caution when applying fenofibrate therapy to the elderly. Full article
(This article belongs to the Special Issue Molecular Mechanisms of the Aging Process)
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Review

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14 pages, 469 KiB  
Review
Accelerated Aging in Cancer Survivors: Cellular Senescence, Frailty, and Possible Opportunities for Interventions
by Shuo Wang, Najla El Jurdi, Bharat Thyagarajan, Anna Prizment and Anne H. Blaes
Int. J. Mol. Sci. 2024, 25(6), 3319; https://doi.org/10.3390/ijms25063319 - 14 Mar 2024
Viewed by 1519
Abstract
The population of cancer survivors has markedly increased due to the rapid improvements in cancer treatment. However, cancer survivors experience accelerated aging, which leads to chronic diseases and other age-related conditions, such as frailty. Those conditions may persist years after cancer diagnosis and [...] Read more.
The population of cancer survivors has markedly increased due to the rapid improvements in cancer treatment. However, cancer survivors experience accelerated aging, which leads to chronic diseases and other age-related conditions, such as frailty. Those conditions may persist years after cancer diagnosis and treatment. Cellular senescence, a hallmark of aging, is one of the mechanisms that contribute to accelerated aging in cancer survivors. Several aging measures, including measures based on clinical markers and biomarkers, have been proposed to estimate the aging process, and some of them have shown associations with mortality and frailty in cancer survivors. Several anti-aging interventions, including lifestyle changes and anti-aging drugs, have been proposed. Future research, particularly in large-scale studies, is needed to determine the efficiency of these aging measures and anti-aging interventions before considering their application in clinics. This review focuses on the mechanisms of cellular senescence and accelerated aging in cancer survivors, assessment of the aging process using clinical markers and biomarkers, and the high prevalence of frailty in that population, as well as possible opportunities for anti-aging interventions. A deeper understanding of aging measures and anti-aging interventions in cancer survivors will contribute to the development of effective strategies to mitigate accelerated aging in cancer survivors and improve their quality of life. Full article
(This article belongs to the Special Issue Molecular Mechanisms of the Aging Process)
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18 pages, 1161 KiB  
Review
Aging, Neurodegenerative Disorders, and Cerebellum
by Igor Y. Iskusnykh, Anastasia A. Zakharova, Evgenii D. Kryl’skii and Tatyana N. Popova
Int. J. Mol. Sci. 2024, 25(2), 1018; https://doi.org/10.3390/ijms25021018 - 13 Jan 2024
Viewed by 2164
Abstract
An important part of the central nervous system (CNS), the cerebellum is involved in motor control, learning, reflex adaptation, and cognition. Diminished cerebellar function results in the motor and cognitive impairment observed in patients with neurodegenerative disorders such as Alzheimer’s disease (AD), vascular [...] Read more.
An important part of the central nervous system (CNS), the cerebellum is involved in motor control, learning, reflex adaptation, and cognition. Diminished cerebellar function results in the motor and cognitive impairment observed in patients with neurodegenerative disorders such as Alzheimer’s disease (AD), vascular dementia (VD), Parkinson’s disease (PD), Huntington’s disease (HD), spinal muscular atrophy (SMA), amyotrophic lateral sclerosis (ALS), Friedreich’s ataxia (FRDA), and multiple sclerosis (MS), and even during the normal aging process. In most neurodegenerative disorders, impairment mainly occurs as a result of morphological changes over time, although during the early stages of some disorders such as AD, the cerebellum also serves a compensatory function. Biological aging is accompanied by changes in cerebellar circuits, which are predominantly involved in motor control. Despite decades of research, the functional contributions of the cerebellum and the underlying molecular mechanisms in aging and neurodegenerative disorders remain largely unknown. Therefore, this review will highlight the molecular and cellular events in the cerebellum that are disrupted during the process of aging and the development of neurodegenerative disorders. We believe that deeper insights into the pathophysiological mechanisms of the cerebellum during aging and the development of neurodegenerative disorders will be essential for the design of new effective strategies for neuroprotection and the alleviation of some neurodegenerative disorders. Full article
(This article belongs to the Special Issue Molecular Mechanisms of the Aging Process)
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