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Aging: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches (2nd Edition)

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 December 2024 | Viewed by 5303

Special Issue Editor

Prof. Dr. Darío Acuña-Castroviejo

E-Mail Website
Guest Editor
Centro de Investigación Biomédica, Instituto de Biotecnología, Parque Tecnológico de Ciencias de la Salud, Universidad de Granada, 18016 Granada, Spain
Interests: melatonin; mitochondria; aging; neurodegeneration; sepsis; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Aging is the gradual deterioration of functional integrity and systemic homeostasis, concluding in death. During the last century, improvements in health care have notably increased the quality and expectancy of life in humans but have consequently led to frailty and morbidity. The complexity of aging is determined by the following hallmarks: chronodisruption, genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. Advances in research have facilitated the identification of genes that regulate aging, such as those implicated in the molecular machinery of the biological clock, nutrient-sensing pathways, growth factor pathways, mitochondria function, inflammation, and the immune system. Human genetic studies, genetically modified mouse models, and studies on the evolution of lifespan in nature have revealed new avenues to understanding the molecular genetics of aging. However, genetic regulation of the elderly remains inscrutable. Furthermore, differences in sex and environmental influences remain unknown and are future challenges within the scientific community. Elucidating the genetic mechanisms that underlie aging is essential for mitigating age-related diseases, reducing fragility, and promoting a healthy human lifespan.

This Special Issue will discuss the current state of the art, challenges, and opportunities in aging. Authors are encouraged to submit original research manuscripts and related review articles.

Prof. Dr. Darío Acuña-Castroviejo
Guest Editor

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

  • human aging
  • molecular clock
  • aging genes
  • epigenetics
  • nutrigenomics
  • inflammaging
  • stem cells
  • telomeres
  • mitochondria

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Related Special Issue

Published Papers (7 papers)

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Research

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12 pages, 1743 KiB  
Article
Immunoaging at Early Ages Could Drive a Higher Comorbidity Burden in People with HIV on Antiretroviral Therapy Compared with the Uninfected Population
by Cora Loste, Macedonia Trigueros, Francisco Muñoz-López, Víctor Urrea, Ana Martínez, Sandra González, Jordi Puig, Marta Martín, Anna Bonjoch, Patricia Echeverría, Marta Massanella and Eugenia Negredo
Int. J. Mol. Sci. 2024, 25(20), 10930; https://doi.org/10.3390/ijms252010930 - 11 Oct 2024
Viewed by 311
Abstract
This is an observational, cross-sectional, comparative case–control, pilot study aimed at assessing the impact of HIV infection and age on immunological markers in people with HIV (PWH) on antiretroviral therapy (ART). The study included 40 PWH on ART, divided into two age groups [...] Read more.
This is an observational, cross-sectional, comparative case–control, pilot study aimed at assessing the impact of HIV infection and age on immunological markers in people with HIV (PWH) on antiretroviral therapy (ART). The study included 40 PWH on ART, divided into two age groups (40–45 years vs. ≥60 years), and 30 HIV-uninfected controls matched by sex and age. The results show that older PWH on ART had more comorbidities and a higher frequency of CD8 T cells compared to older controls, with a significant decrease in CD8 naïve T cells with age. Additionally, younger PWH on ART exhibited higher frequencies of activated CD8 T cells and elevated levels of inflammatory markers (sCD14, IL-6) compared to age-matched controls, with values similar to those of older PWH on ART. These findings suggest that younger PWH on ART may experience accelerated immunoaging, highlighting the need for early interventions in this population. Full article
(This article belongs to the Special Issue Aging: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches (2nd Edition))
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20 pages, 4536 KiB  
Article
Lifespan Extension by Retrotransposons under Conditions of Mild Stress Requires Genes Involved in tRNA Modifications and Nucleotide Metabolism
by Patrick H. Maxwell, Mustafa Mahmood, Maya Villanueva, Kaitlyn Devine and Nina Avery
Int. J. Mol. Sci. 2024, 25(19), 10593; https://doi.org/10.3390/ijms251910593 - 1 Oct 2024
Viewed by 403
Abstract
Retrotransposons are mobile DNA elements that are more active with increasing age and exacerbate aging phenotypes in multiple species. We previously reported an unexpected extension of chronological lifespan in the yeast, Saccharomyces paradoxus, due to the presence of Ty1 retrotransposons when cells [...] Read more.
Retrotransposons are mobile DNA elements that are more active with increasing age and exacerbate aging phenotypes in multiple species. We previously reported an unexpected extension of chronological lifespan in the yeast, Saccharomyces paradoxus, due to the presence of Ty1 retrotransposons when cells were aged under conditions of mild stress. In this study, we tested a subset of genes identified by RNA-seq to be differentially expressed in S. paradoxus strains with a high-copy number of Ty1 retrotransposons compared with a strain with no retrotransposons and additional candidate genes for their contribution to lifespan extension when cells were exposed to a moderate dose of hydroxyurea (HU). Deletion of ADE8, NCS2, or TRM9 prevented lifespan extension, while deletion of CDD1, HAC1, or IRE1 partially prevented lifespan extension. Genes overexpressed in high-copy Ty1 strains did not typically have Ty1 insertions in their promoter regions. We found that silencing genomic copies of Ty1 prevented lifespan extension, while expression of Ty1 from a high-copy plasmid extended lifespan in medium with HU or synthetic medium. These results indicate that cells adapt to expression of retrotransposons by changing gene expression in a manner that can better prepare them to remain healthy under mild stress. Full article
(This article belongs to the Special Issue Aging: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches (2nd Edition))
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11 pages, 1362 KiB  
Article
The Oldest of Old Male C57B/6J Mice Are Protected from Sarcopenic Obesity: The Possible Role of Skeletal Muscle Protein Kinase B Expression
by Thomas H. Reynolds IV, Noa Mills, Dakembay Hoyte, Katy Ehnstrom and Alex Arata
Int. J. Mol. Sci. 2024, 25(19), 10278; https://doi.org/10.3390/ijms251910278 - 24 Sep 2024
Viewed by 668
Abstract
The impact of aging on body composition and glucose metabolism is not well established in C57BL/6J mice, despite being a common pre-clinical model for aging and metabolic research. The purpose of this study was to examine the effect of advancing age on body [...] Read more.
The impact of aging on body composition and glucose metabolism is not well established in C57BL/6J mice, despite being a common pre-clinical model for aging and metabolic research. The purpose of this study was to examine the effect of advancing age on body composition, in vivo glucose metabolism, and skeletal muscle AKT expression in young (Y: 4 months old, n = 7), old (O: 17–18 months old, n = 10), and very old (VO: 26–27 month old, n = 9) male C57BL/6J mice. Body composition analysis, assessed by nuclear magnetic resonance, demonstrated O mice had a significantly greater fat mass and body fat percentage when compared to Y and VO mice. Furthermore, VO mice had a significantly greater lean body mass than both O and Y mice. We also found that the VO mice had greater AKT protein levels in skeletal muscle compared to O mice, an observation that explains a portion of the increased lean body mass in VO mice. During glucose tolerance (GT) testing, blood glucose values were significantly lower in the VO mice when compared to the Y and O mice. No age-related differences were observed in insulin tolerance (IT). We also assessed the glucose response to AMPK activation by 5-aminoimidazole-4-carboxamide-1-β-D-ribofuranoside (AICAR). The change in blood glucose following AICAR administration was significantly reduced in VO mice compared to Y and AG mice. Our findings indicate that lean body mass and AKT2 protein expression in muscle are significantly increased in VO mice compared to O mice. The increase in AKT2 likely plays a role in the greater lean body mass observed in the oldest of old mice. Finally, despite the increased GT, VO mice appear to be resistant to AMPK-mediated glucose uptake. Full article
(This article belongs to the Special Issue Aging: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches (2nd Edition))
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16 pages, 5269 KiB  
Article
The Interstitial Gland as a Source of Pro- or Anti-Senescent Cells during Chinchilla Rabbit Ovarian Aging
by Verónica Díaz-Hernández, Alejandro Marmolejo-Valencia, César Montiel-De la Cruz, Gabriela Piñón-Zárate, Luis M. Montaño, Silvia Ivonne Mora-Herrera and Ivette Caldelas
Int. J. Mol. Sci. 2024, 25(18), 9906; https://doi.org/10.3390/ijms25189906 - 13 Sep 2024
Viewed by 655
Abstract
The aging ovary in mammals leads to the reduced production of sex hormones and a deterioration in follicle quality. The interstitial gland originates from the hypertrophy of the theca cells of atretic follicles and represents an accumulative structure of the ovary that may [...] Read more.
The aging ovary in mammals leads to the reduced production of sex hormones and a deterioration in follicle quality. The interstitial gland originates from the hypertrophy of the theca cells of atretic follicles and represents an accumulative structure of the ovary that may contribute to its aging. Here, reproductive and mature rabbit ovaries are used to determine whether the interstitial gland plays a crucial role in ovarian aging. We demonstrate that, in the mature ovary, interstitial gland cells accumulate lipid droplets and show ultrastructural characteristics of lipophagy. Furthermore, they undergo modifications and present a foamy appearance, do not express the pan-leukocyte CD-45 marker, and express CYP11A1. These cells are the first to present an increase in lipofuscin accumulation. In foamy cells, the expression of p21 remains low, PCNA expression is maintained at mature ages, and their nuclei do not show positivity for H2AX. The interstitial gland shows a significant increase in lipofuscin accumulation compared with the ovaries of younger rabbits, but lipofuscin accumulation remains constant at mature ages. Surprisingly, no accumulation of cells with DNA damage is evident, and an increase in proliferative cells is observed at the age of 36 months. We suggest that the interstitial gland initially uses lipophagy to maintain steroidogenic homeostasis and prevent cellular senescence. Full article
(This article belongs to the Special Issue Aging: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches (2nd Edition))
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11 pages, 3717 KiB  
Article
Alterations of Liver Morphology in Senescent Rats
by Ruth Maldonado-Rengel, Zaida Sócola-Barsallo and Bélgica Vásquez
Int. J. Mol. Sci. 2024, 25(18), 9846; https://doi.org/10.3390/ijms25189846 - 12 Sep 2024
Viewed by 324
Abstract
Age-related liver changes can have important implications for health and metabolic function. This study aimed to describe the morphoquantitative alterations of the liver in senescent rats compared to adult rats. Twelve male rats were used, divided into 6-month-old adults (group A) and 36-month-old [...] Read more.
Age-related liver changes can have important implications for health and metabolic function. This study aimed to describe the morphoquantitative alterations of the liver in senescent rats compared to adult rats. Twelve male rats were used, divided into 6-month-old adults (group A) and 36-month-old senescent rats (group S). Morphometric and histopathological studies, quantification of collagen types I and III, and stereological analyses were performed to determine the volume density of mononucleated (VvhepM) and binucleated (VvhepB) hepatocyte nuclei, surface area density (SvhepM), and number density (NvhepM) of mononucleated hepatocyte nuclei. The findings reveal an alteration of the normal liver tissue architecture in senescent rats and the presence of inflammatory lesions and fibrosis. In addition, there was a decrease in body and liver mass and volume. Group S showed a significant reduction in VvhepM and NvhepM; however, SvhepM was significantly higher. No significant differences were noted in the percentage of binucleated hepatocytes between the two groups. This study reveals substantial morphological changes in the aging liver, with possible functional implications. More research is needed on the underlying mechanisms and their consequences at older ages. Full article
(This article belongs to the Special Issue Aging: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches (2nd Edition))
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14 pages, 1600 KiB  
Article
Moderate Aerobic Exercise Induces Homeostatic IgA Generation in Senile Mice
by Angel J. Hernández-Urbán, Maria-Elisa Drago-Serrano, Aldo A. Reséndiz-Albor, José A. Sierra-Ramírez, Fabiola Guzmán-Mejía, Rigoberto Oros-Pantoja and Marycarmen Godínez-Victoria
Int. J. Mol. Sci. 2024, 25(15), 8200; https://doi.org/10.3390/ijms25158200 - 27 Jul 2024
Viewed by 765
Abstract
A T-cell-independent (TI) pathway activated by microbiota results in the generation of low-affinity homeostatic IgA with a critical role in intestinal homeostasis. Moderate aerobic exercise (MAE) provides a beneficial impact on intestinal immunity, but the action of MAE on TI-IgA generation under senescence [...] Read more.
A T-cell-independent (TI) pathway activated by microbiota results in the generation of low-affinity homeostatic IgA with a critical role in intestinal homeostasis. Moderate aerobic exercise (MAE) provides a beneficial impact on intestinal immunity, but the action of MAE on TI-IgA generation under senescence conditions is unknown. This study aimed to determine the effects of long-term MAE on TI-IgA production in young (3 month old) BALB/c mice exercised until adulthood (6 months) or aging (24 months). Lamina propria (LP) from the small intestine was obtained to determine B cell and plasma cell sub-populations by flow cytometry and molecular factors related to class switch recombination [Thymic Stromal Lymphopoietin (TSLP), A Proliferation-Inducing Ligand (APRIL), B Cell Activating Factor (BAFF), inducible nitric oxide synthase (iNOS), and retinal dehydrogenase (RDH)] and the synthesis of IgA [α-chain, interleukin (IL)-6, IL-21, and Growth Factor-β (TGF-β)]; and epithelial cells evaluated IgA transitosis [polymeric immunoglobulin receptor (pIgR), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), IL-4] by the RT-qPCR technique. The results were compared with data obtained from sedentary age-matched mice. Statistical analysis was computed with ANOVA, and p < 0.05 was considered to be a statistically significant difference. Under senescence conditions, MAE promoted the B cell and IgA+ B cells and APRIL, which may improve the intestinal response and ameliorate the inflammatory environment associated presumably with the downmodulation of pro-inflammatory mediators involved in the upmodulation of pIgR expression. Data suggested that MAE improved IgA and downmodulate the cytokine pro-inflammatory expression favoring homeostatic conditions in aging. Full article
(This article belongs to the Special Issue Aging: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches (2nd Edition))
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Review

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23 pages, 1211 KiB  
Review
mTOR and SGLT-2 Inhibitors: Their Synergistic Effect on Age-Related Processes
by Dario Troise, Silvia Mercuri, Barbara Infante, Vincenzo Losappio, Luciana Cirolla, Giuseppe Stefano Netti, Elena Ranieri and Giovanni Stallone
Int. J. Mol. Sci. 2024, 25(16), 8676; https://doi.org/10.3390/ijms25168676 - 8 Aug 2024
Viewed by 1688
Abstract
The aging process contributes significantly to the onset of chronic diseases, which are the primary causes of global mortality, morbidity, and healthcare costs. Numerous studies have shown that the removal of senescent cells from tissues extends lifespan and reduces the occurrence of age-related [...] Read more.
The aging process contributes significantly to the onset of chronic diseases, which are the primary causes of global mortality, morbidity, and healthcare costs. Numerous studies have shown that the removal of senescent cells from tissues extends lifespan and reduces the occurrence of age-related diseases. Consequently, there is growing momentum in the development of drugs targeting these cells. Among them, mTOR and SGLT-2 inhibitors have garnered attention due to their diverse effects: mTOR inhibitors regulate cellular growth, metabolism, and immune responses, while SGLT-2 inhibitors regulate glucose reabsorption in the kidneys, resulting in various beneficial metabolic effects. Importantly, these drugs may act synergistically by influencing senescence processes and pathways. Although direct studies on the combined effects of mTOR inhibition and SGLT-2 inhibition on age-related processes are limited, this review aims to highlight the potential synergistic benefits of these drugs in targeting senescence. Full article
(This article belongs to the Special Issue Aging: From Molecular Mechanisms, Pathophysiology to Novel Therapeutic Approaches (2nd Edition))
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