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Molecular Studies in Aging, 2nd Edition
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Molecular Studies in Aging, 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 13671

Special Issue Editor

Dr. Rosa Mancinelli

E-Mail Website
Guest Editor
Department of Neuroscience, Imaging and Clinical Sciences, University ”G. d’Annunzio” Chieti-Pescara, 66100 Chieti, Italy
Interests: muscle stem cells; molecular biology; skeletal muscle regeneration
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The perspective regarding the lengthening of life raises the fundamental issue of aging in good health, with autonomy and independence, both for the quality of life and the containment of health care costs. This represents a challenge to maintaining efficient tissues, organs, and systems of the body.

Lifestyle and environmental factors play a preponderant role during the early stages of life, while genetics become fundamental to establish the complete life span of an organism.

Today, several approaches are used to both study and better understand the mechanisms underlying the aging processes, as well as to counteract and decelerate them. There are several tissues and systems that undergo aging, and among those most affected are the muscle, bone, nervous system, and cardiovascular system. The rationale of this Special Issue is essentially to collect new discoveries and study approaches on aging processes at the molecular, cellular, and integrative levels, as well as new proposals for the achievement of active aging (for example, mind training, physical activity, and diet).

We have already published 8 papers in Volume I. In Volume II, we invite researchers to provide original research articles and review articles regarding results in the field of the new frontiers that can contribute to the understanding of aging processes and the prospect of healthy old age.

Dr. Rosa Mancinelli
Guest Editor

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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 250 words) can be sent to the Editorial Office for assessment.

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.

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Keywords

  • senescence
  • active aging
  • sarcopenia
  • osteoporosis
  • oxidative stress
  • brain aging
  • cardiovascular aging

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Published Papers (6 papers)

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Research

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19 pages, 2280 KB  
Article
Age- and Genotype-Associated Specific Expression of IL-1 and TNF Receptors on Immunocompetent Cells
by Julia Zhukova, Julia Lopatnikova, Filipp Vasilyev, Alina Alshevskaya, Darya Lipa and Sergey Sennikov
Int. J. Mol. Sci. 2026, 27(2), 807; https://doi.org/10.3390/ijms27020807 - 13 Jan 2026
Viewed by 515
Abstract
Aging is accompanied by a chronic, low-grade inflammatory state known as “inflammaging,” largely driven by dysregulated signaling of pro-inflammatory cytokines like IL-1 and TNF-α. The biological impact of these cytokines is modulated by the expression of their cellular receptors, which is influenced by [...] Read more.
Aging is accompanied by a chronic, low-grade inflammatory state known as “inflammaging,” largely driven by dysregulated signaling of pro-inflammatory cytokines like IL-1 and TNF-α. The biological impact of these cytokines is modulated by the expression of their cellular receptors, which is influenced by genetic polymorphisms. However, the interplay between age, genetic variation, and cell-type-specific receptor expression remains incompletely characterized. This study aimed to determine the relative and absolute expression levels of IL-1 and TNF receptors on major immunocompetent cell populations in healthy donors of different age groups and to assess the influence of receptor gene polymorphisms on this expression. A cohort of 144 healthy donors was stratified into two age clusters using unsupervised clustering: a “young” group (18–31 years, n = 71) and an “older” group (32–59 years, n = 73). Membrane expression of TNFR1, TNFR2, IL-1R1, and IL-1R2 on T-lymphocytes, B-lymphocytes, and monocytes was analyzed by flow cytometry. The analysis included both the percentage of receptor-positive cells and the number of receptors per cell using absolute quantification with calibration beads. Genotyping for eight SNPs in the TNF1, TNFR2, IL1R1, and IL1R2 genes was performed via PCR-RFLP. The most pronounced age-related differences were observed in monocytes, in which the young cohort exhibited a significantly higher percentage of TNFR1- and TNFR2-positive monocytes, as well as a higher number of IL-1R1 receptors. In contrast, T-lymphocytes from the older cluster showed a higher percentage of TNFR2-positive cells. Genetic polymorphisms significantly modulated receptor expression in an age-dependent manner. For example, in the young cluster, polymorphisms primarily affected receptor levels on B-lymphocytes, whereas in the older cluster, the most significant associations were observed in monocytes. This study reveals significant, cell-specific alterations in the IL-1 and TNF receptor landscapes with age, with monocytes being particularly affected. The observed receptor downregulation in older adults is likely to reflect an active process of ligand-induced desensitization driven by chronic inflammation. Furthermore, genetic polymorphisms exert age-dependent effects on receptor expression, highlighting the dynamic interplay between genetics and immunosenescence. These findings provide a foundation for personalized strategies to mitigate inflammaging. Full article
(This article belongs to the Special Issue Molecular Studies in Aging, 2nd Edition)
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18 pages, 1485 KB  
Article
Probiotic Modulation in Aging: Strain-Specific Geroprotective Effects in Caenorhabditis elegans
by Barbara Sciandrone, Diletta Francesca Squarzanti, Patrizia Malfa and Maria Elena Regonesi
Int. J. Mol. Sci. 2025, 26(22), 11205; https://doi.org/10.3390/ijms262211205 - 20 Nov 2025
Cited by 1 | Viewed by 1528
Abstract
Elderly individuals are more vulnerable to disease due to their increased frailty. Emerging evidence highlights the potential of probiotics as geroprotective agents by maintaining gut health and modulating key physiological processes involved in aging, such as inflammation, cognitive functions, and metabolism. Here, we [...] Read more.
Elderly individuals are more vulnerable to disease due to their increased frailty. Emerging evidence highlights the potential of probiotics as geroprotective agents by maintaining gut health and modulating key physiological processes involved in aging, such as inflammation, cognitive functions, and metabolism. Here, we investigated the geroprotective potential of four probiotic strains (Lacticaseibacillus paracasei LPC1114, Limosilactobacillus reuteri PBS072, Bifidobacterium breve BB077, and Bifidobacterium animalis subsp. lactis BL050) using Caenorhabditis elegans as an aging model. Mid-life healthspan parameters were assessed, including lifespan, motility, ROS levels, lipofuscin accumulation, and cognitive capabilities. The probiotics exhibited strain-specific effects. L. reuteri PBS072 and B. lactis BL050 significantly increased locomotion by 20% and decreased ROS levels by 70% and 30% respectively, suggesting enhanced oxidative stress response and neuromuscular maintenance. B. breve BB077, L. paracasei LPC1114, and L. reuteri PBS072 enhanced associative learning performance, whereas B. lactis BL050 improved chemotactic response. Notably, only L. paracasei LPC1114 and L. reuteri PBS072 extended the maximum lifespan by 4 and 5 days, respectively, an effect mediated by the longevity-related genes skn1, sir2.1, and daf16. Our findings highlight the multifaceted, strain-specific geroprotective properties of probiotics and support their potential as microbiome-based interventions to promote healthy aging. Full article
(This article belongs to the Special Issue Molecular Studies in Aging, 2nd Edition)
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16 pages, 1670 KB  
Article
Role of Repeat Tract Structure and the rs7158733 SNP in Spinocerebellar Ataxia 3
by Suran Nethisinghe, Hector Garcia-Moreno, Jude Alwan, Robyn Labrum and Paola Giunti
Int. J. Mol. Sci. 2025, 26(20), 9836; https://doi.org/10.3390/ijms26209836 - 10 Oct 2025
Viewed by 1411
Abstract
Spinocerebellar ataxia 3 (SCA3) is a neurodegenerative condition caused by an expansion of a polyglutamine tract within the ATXN3 gene. Normal alleles range from 12 to 44 repeats, while pathogenic alleles have 52 repeats or more. The canonical ATXN3 repeat tract sequence includes [...] Read more.
Spinocerebellar ataxia 3 (SCA3) is a neurodegenerative condition caused by an expansion of a polyglutamine tract within the ATXN3 gene. Normal alleles range from 12 to 44 repeats, while pathogenic alleles have 52 repeats or more. The canonical ATXN3 repeat tract sequence includes three interruptions at positions 3 (CAA), 4 (AAG), and 6 (CAA). The intragenic rs7158733 single-nucleotide polymorphism (SNP) flanks the ATXN3 repeat region and substitutes a TAC1118 tyrosine codon with a TAA1118 stop codon, resulting in a shorter ataxin-3aS isoform. We examined the distribution of SCA3 allele repeat sizes in a UK-based cohort presenting with an ataxic phenotype. The 6596 alleles showed a clear gap between normal and expanded alleles, with no intermediate alleles containing 41 to 57 repeats. We used clone sequencing to characterize the structure of the ATXN3 repeat region in a sub-cohort of 44 SCA3 patients. We observed that the three canonical interruptions were typically preserved. There was no association of the interruptions with age at onset detected in this cohort, given the limited power of this sub-cohort. We genotyped the rs7158733 SNP in a sub-cohort of 79 SCA3 patients and found that 74.7% of expanded alleles carried the A1118 variant, which was associated with earlier disease onset. This study highlights the importance of rs7158733 genotyping alongside ATXN3 repeat sizing for patient evaluation, as this SNP modifies the effect of repeat size on age at onset in SCA3 for pathogenic alleles up to 69 repeats. Full article
(This article belongs to the Special Issue Molecular Studies in Aging, 2nd Edition)
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15 pages, 2826 KB  
Article
Ajuba as a Potential Nutrition-Responsive Biomarker for the Prevention of Age-Related Sarcopenia
by Youngji Han and Seung Pil Pack
Int. J. Mol. Sci. 2025, 26(16), 7869; https://doi.org/10.3390/ijms26167869 - 14 Aug 2025
Viewed by 1264
Abstract
Sarcopenia, the age-related decline in skeletal muscle mass and function, is a growing health concern in aging populations. Nutritional interventions are increasingly recognized for their therapeutic potential; however, molecular biomarkers that reflect their efficacy are limited. To identify nutrition-responsive genes relevant to sarcopenia, [...] Read more.
Sarcopenia, the age-related decline in skeletal muscle mass and function, is a growing health concern in aging populations. Nutritional interventions are increasingly recognized for their therapeutic potential; however, molecular biomarkers that reflect their efficacy are limited. To identify nutrition-responsive genes relevant to sarcopenia, we performed transcriptomic profiling of gastrocnemius muscle from mature and middle-aged mice. Aging-associated differentially expressed genes (DEGs) were filtered based on expression levels and correlation with muscle mass. Functional food interventions, including high- and low-molecular-weight collagen hydrolysates and allulose, were applied, and effect scores were calculated to assess transcriptomic responsiveness. Ajuba, a gene involved in cytoskeletal regulation and tissue remodeling, was significantly downregulated in middle-aged mice, consistent with aging-associated muscle decline. Dietary supplementation restored Ajuba expression across all intervention groups, with the strongest effect observed in the high-molecular-weight collagen group. Ajuba expression also showed strong positive correlations with tibialis anterior mass, hindlimb thickness, and muscle-to-fat ratio. Ajuba was identified as a nutritionally modifiable gene with strong associations to muscle phenotype and dietary response. These findings support Ajuba as a transcriptomic biomarker and potential molecular target for precision nutrition strategies aimed at preventing or mitigating sarcopenia. Full article
(This article belongs to the Special Issue Molecular Studies in Aging, 2nd Edition)
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Review

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16 pages, 551 KB  
Review
Degradation of the Molecular Basis of Life During the Aging Process
by Janusz Wiesław Błaszczyk
Int. J. Mol. Sci. 2026, 27(5), 2419; https://doi.org/10.3390/ijms27052419 - 6 Mar 2026
Viewed by 666
Abstract
Aging is a chronic, destructive process characterized by the progressive breakdown of the body, leading to a loss of control over homeostasis. Glucose is the most important metabolite involved in metabolism and maintaining homeostasis in the human body. Glucose-based energy metabolism is fundamental [...] Read more.
Aging is a chronic, destructive process characterized by the progressive breakdown of the body, leading to a loss of control over homeostasis. Glucose is the most important metabolite involved in metabolism and maintaining homeostasis in the human body. Glucose-based energy metabolism is fundamental to the activity and structural changes in the brain, which is the main regulator of life processes. Disturbances in energy metabolism and glucose-dependent metabolic processes have a decisive impact on the aging process. Age-related deficiency of the coenzyme NAD, which regulates glucose metabolism in neurons, leads to irreversible changes in the brain, culminating in senescence. Research on NAD precursors offers hope that although we cannot completely halt the aging process, NAD supplementation may enable healthy aging. Full article
(This article belongs to the Special Issue Molecular Studies in Aging, 2nd Edition)
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29 pages, 916 KB  
Review
Multiomics of Aging and Aging-Related Diseases
by Olga I. Kiseleva, Viktoriia A. Arzumanian, Yuriy A. Ikhalaynen, Ilya Y. Kurbatov, Polina A. Kryukova and Ekaterina V. Poverennaya
Int. J. Mol. Sci. 2024, 25(24), 13671; https://doi.org/10.3390/ijms252413671 - 21 Dec 2024
Cited by 7 | Viewed by 6975
Abstract
Despite their astonishing biological diversity, surprisingly few shared traits connect all or nearly all living organisms. Aging, i.e., the progressive and irreversible decline in the function of multiple cells and tissues, is one of these fundamental features of all organisms, ranging from single-cell [...] Read more.
Despite their astonishing biological diversity, surprisingly few shared traits connect all or nearly all living organisms. Aging, i.e., the progressive and irreversible decline in the function of multiple cells and tissues, is one of these fundamental features of all organisms, ranging from single-cell creatures to complex animals, alongside variability, adaptation, growth, healing, reproducibility, mobility, and, finally, death. Age is a key determinant for many pathologies, shaping the risks of incidence, severity, and treatment outcomes for cancer, neurodegeneration, heart failure, sarcopenia, atherosclerosis, osteoporosis, and many other diseases. In this review, we aim to systematically investigate the age-related features of the development of several diseases through the lens of multiomics: from genome instability and somatic mutations to pathway alterations and dysregulated metabolism. Full article
(This article belongs to the Special Issue Molecular Studies in Aging, 2nd Edition)
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