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Molecular Mechanisms of the Aging Process: 2nd Edition
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Molecular Mechanisms of the Aging Process: 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 September 2026 | Viewed by 10105

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,

This Special Issue is the continuation of our Special Issue “Molecular Mechanisms of the Aging Process” (https://www.mdpi.com/journal/ijms/special_issues/SB61B421T6).

Over the past decade, research on the molecular mechanisms of aging has surged, including the discovery of the epigenetic clock as a potential biomarker of aging and pioneering work on using 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. They are 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 hallmarks of aging in order to determine their individual contributions to the overall process and enable the development of new therapies that may ameliorate or slow aging in humans. Lifestyle interventions such as calorie restriction and exercise, along with small-molecule therapies, have shown increasing promise potential treatments to improve healthspan and combat age-related diseases.

We invite you to explore recent advancements in the vast field of aging research. This Special Issue welcomes original research articles, mini and full reviews, and perspectives that address the progress and current state of molecular mechanisms underlying the aging process, particularly in the following areas:

  • 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 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-anonymized 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 process
  • molecular mechanisms
  • epigenetic clock
  • cancer
  • metabolic disease

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Published Papers (2 papers)

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Review

32 pages, 5202 KB  
Review
Epigenetic Age Acceleration as a Modifiable Public Health Target: A Systematic Review and Meta-Analysis of Environmental, Behavioral, and Social Determinants with Development of the MEAB-Index
by Silvana Mirella Aliberti, Piergiorgio Marigliano and Mario Capunzo
Int. J. Mol. Sci. 2026, 27(11), 5032; https://doi.org/10.3390/ijms27115032 - 2 Jun 2026
Viewed by 1111
Abstract
Chronological age is a poor indicator of interindividual differences in biological aging. DNA methylation-based epigenetic clocks provide a reliable measure of biological age and epigenetic age acceleration (EAA). Although modifiable behavioral, environmental, and social factors appear to influence EAA, the magnitude, consistency, and [...] Read more.
Chronological age is a poor indicator of interindividual differences in biological aging. DNA methylation-based epigenetic clocks provide a reliable measure of biological age and epigenetic age acceleration (EAA). Although modifiable behavioral, environmental, and social factors appear to influence EAA, the magnitude, consistency, and potential preventability of these associations have never been systematically quantified. We conducted a systematic review and meta-analysis following PRISMA 2020 guidelines. PubMed/MEDLINE and Scopus were searched from inception to 7 April 2026 for English-language observational and interventional studies reporting quantitative associations between modifiable determinants and EAA measured using validated clocks (Horvath, PhenoAge, GrimAge, DunedinPACE). Effect sizes were harmonized into four analytical pools. Random-effects meta-analyses were performed using the DerSimonian–Laird estimator, with pre-specified subgroup analyses by exposure category. Heterogeneity, publication bias, and robustness were thoroughly assessed. A novel Modifiable Epigenetic Aging Burden Index (MEAB-Index) was developed to quantify the cumulative preventable burden. Only studies conducted in adult populations (≥18 years) were eligible. Eighty-three studies providing 118 distinct exposure–clock associations were included. In the primary analysis (Pool A, n = 60), adverse modifiable exposures were associated with accelerated EAA (pooled β = +0.310 years per unit exposure, 95% CI 0.255–0.366). The strongest associations were observed for metabolic and inflammatory markers (β = +0.913) and environmental exposures (β = +0.466). The MEAB-Index yielded a Cumulative Preventable Burden of +1.566 years (bootstrap 95% CI 1.011–2.123). Findings were robust across sensitivity analyses and remained directionally consistent in secondary pools (B–D). This study provides the most comprehensive quantitative synthesis to date on the modifiability of epigenetic aging. Our findings demonstrate that EAA is meaningfully shaped by behavioral, environmental, and social determinants. The MEAB-Index introduces a novel framework for estimating the preventable burden of biological aging and for prioritizing interventions. Reducing key modifiable risk factors, particularly metabolic/inflammatory and environmental exposures, could substantially slow biological aging at the population level and support the transition toward ageing-centered preventive strategies. Full article
(This article belongs to the Special Issue Molecular Mechanisms of the Aging Process: 2nd Edition)
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31 pages, 2341 KB  
Review
Sarcopenia in the Aging Process: Pathophysiological Mechanisms, Clinical Implications, and Emerging Therapeutic Approaches
by Larissa Parreira Araújo, Ana Clara Figueiredo Godoy, Fernanda Fortes Frota, Caroline Barbalho Lamas, Karina Quesada, Claudia Rucco Penteado Detregiachi, Adriano Cressoni Araújo, Maria Angélica Miglino, Elen Landgraf Guiguer, Rafael Santos de Argollo Haber, Eliana de Souza Bastos Mazuqueli Pereira, Virgínia Cavallari Strozze Catharin, Vitor Cavallari Strozze Catharin, Lucas Fornari Laurindo and Sandra Maria Barbalho
Int. J. Mol. Sci. 2025, 26(24), 12147; https://doi.org/10.3390/ijms262412147 - 17 Dec 2025
Cited by 18 | Viewed by 8430
Abstract
In the face of population aging, sarcopenia has emerged as a significant muscle disorder characterized by the progressive loss of muscle mass, strength, and function. Chronic inflammation, oxidative stress, and mitochondrial dysfunction contribute to sarcopenia and help explain its association with comorbidities such [...] Read more.
In the face of population aging, sarcopenia has emerged as a significant muscle disorder characterized by the progressive loss of muscle mass, strength, and function. Chronic inflammation, oxidative stress, and mitochondrial dysfunction contribute to sarcopenia and help explain its association with comorbidities such as type 2 diabetes, obesity, and neurodegenerative diseases. Despite extensive research, there remains a need to integrate current knowledge on interventions that target these interconnected mechanisms. This review synthesizes recent evidence on the effects of resistance exercise, nutritional supplementation (high-protein intake, leucine, vitamin D, omega-3 fatty acids), and probiotic use on muscle function and inflammatory status in older adults with sarcopenia. Literature was critically analyzed to evaluate the efficacy of multicomponent strategies. The reviewed studies consistently report that combining resistance training with anti-inflammatory nutrition and targeted supplementation improves muscle strength, reduces pro-inflammatory cytokines, and supports mitochondrial function. These findings suggest that an integrated, multicomponent approach represents a promising strategy for attenuating the progression of sarcopenia and reducing its associated comorbidities. Full article
(This article belongs to the Special Issue Molecular Mechanisms of the Aging Process: 2nd Edition)
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