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Cells
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Understanding Aging Mechanisms to Prevent Age-Related Diseases: 2nd Edition
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Understanding Aging Mechanisms to Prevent Age-Related Diseases: 2nd Edition

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

Deadline for manuscript submissions: closed (31 December 2025) | Viewed by 8087

Special Issue Editors

Dr. Gérard Lizard

E-Mail Website
Guest Editor
Team "Biochemistry of the Peroxisome, Inflammation and Lipid Metabolism", Université de Bourgogne, 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
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; aging process; epidemiology; successful aging
Special Issues, Collections and Topics in MDPI journals
Dr. Anne Vejux

E-Mail Website
Guest Editor
Equipe 5, Neurobiologie des Comportements Alimentaires/Neurobiology of Feeding Behaviours 9E, Boulevard Jeanne d'Arc, 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
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

Special Issue Information

Dear Colleagues, 

This is the second edition of “Understanding Aging Mechanisms to Prevent Age-Related Diseases” that previously published ten papers.

During recent decades, the percentage of people over 65 years old, 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 are public health issues. 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 that slow down 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 studies dealing with cellular, molecular, pharmacological, and nutritional aspects of aging and age-related diseases. We look forward to your submissions.

Dr. Gérard Lizard
Prof. Dr. Pierre Jouanny
Dr. Anne Vejux
Prof. Dr. Sonia Hammami
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-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.

Keywords

  • aging
  • age-related diseases
  • pathophysiology
  • cell mechanisms
  • therapies
  • biomarkers

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Related Special Issue

Published Papers (4 papers)

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Research

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12 pages, 1094 KB  
Article
A20 and TNIP-3 Reduce NF-κB-Mediated Paracrine Responses to Hypoxia/Hyperglycemia-Induced Endothelial Senescence
by Lara Russo, Serena Babboni, Serena Del Turco and Giuseppina Basta
Cells 2025, 14(23), 1908; https://doi.org/10.3390/cells14231908 - 2 Dec 2025
Viewed by 867
Abstract
Background: Hypoxia and ageing both involve impaired oxygen delivery, leading to oxidative damage, and endothelial cell (EC) dysfunction. In the presence of chronic hyperglycemia, these effects are amplified, accelerating EC senescence and vascular impairment. Methods: We assessed key mediators of inflammatory signalling and [...] Read more.
Background: Hypoxia and ageing both involve impaired oxygen delivery, leading to oxidative damage, and endothelial cell (EC) dysfunction. In the presence of chronic hyperglycemia, these effects are amplified, accelerating EC senescence and vascular impairment. Methods: We assessed key mediators of inflammatory signalling and senescence, as well as transcriptional regulators responsive to oxidative stress in ECs exposed to high glucose (30.5 mmol/L) for 72 h under either normoxia (21% O2) or prolonged (16 h) hypoxia (2% O2) followed by 2 h of reoxygenation. Results: ECs exposed to high glucose and hypoxia developed a senescent phenotype, as indicated by increased expression of p21 and p16, and elevated β-galactosidase staining. Interestingly, hypoxia-induced senescence did not coincide with the classical senescence-associated secretory phenotype (SASP). Compared to normoxia, ECs exposed to hypoxia, particularly under high-glucose conditions, showed reduced NF-κB-driven proinflammatory secretome (MCP-1, IL-6, IL-8), downregulation of the NF-κB p50 subunit, and simultaneous upregulation of the angiogenic factor VEGF-A with downregulation of YAP-1, a key regulator of cell survival. Notably, we observed a strong upregulation of A20 and TNIP-3, two well-characterized negative regulators of NF-κB signalling. Conclusions: Hypoxia-induced senescence did not trigger a typical inflammatory SASP. Although ECs enter a senescent state, they activate an anti-inflammatory response, suppressing NF-κB signalling and increasing the expression of its inhibitors, A20 and TNIP-3. This may reflect a non-canonical senescence response whose functional significance remains to be determined. Full article
(This article belongs to the Special Issue Understanding Aging Mechanisms to Prevent Age-Related Diseases: 2nd Edition)
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Review

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21 pages, 1763 KB  
Review
Peroxisomes in Aging: Guardians of Cellular Resilience and Function
by Artuur Vercaemst, Mingming Zhao, Ruizhi Chai, Celien Lismont and Marc Fransen
Cells 2026, 15(3), 254; https://doi.org/10.3390/cells15030254 - 28 Jan 2026
Viewed by 809
Abstract
Peroxisomes are multifunctional organelles that play essential roles in lipid metabolism, redox regulation, and cellular signaling. An expanding body of evidence implicates peroxisomal dysfunction as a key contributor to aging and age-related diseases. Aging is accompanied by progressive declines in key peroxisomal functions, [...] Read more.
Peroxisomes are multifunctional organelles that play essential roles in lipid metabolism, redox regulation, and cellular signaling. An expanding body of evidence implicates peroxisomal dysfunction as a key contributor to aging and age-related diseases. Aging is accompanied by progressive declines in key peroxisomal functions, including catalase activity, fatty acid β-oxidation, plasmalogen biosynthesis, and the metabolism of bile acids and docosahexaenoic acid, resulting in increased oxidative stress, lipid dysregulation, and alterations in membrane composition. Impaired pexophagy further exacerbates these defects by allowing the accumulation of damaged peroxisomes and compromising cellular homeostasis. Through extensive metabolic and signaling crosstalk with mitochondria, the endoplasmic reticulum, and lysosomes, peroxisomal dysfunction can propagate oxidative and metabolic disturbances throughout the cell. In addition, peroxisome-derived signaling molecules, such as hydrogen peroxide and bioactive lipids, link peroxisomal activity to cellular stress responses and organismal metabolic homeostasis. We propose that aging-associated impairments in peroxisomal protein import, redox regulation, and selective turnover progressively shift peroxisomes from adaptive metabolic signaling hubs toward sources of chronic oxidative and lipid stress. In this context, current studies highlight peroxisomal homeostasis as a potential determinant of healthy aging and point to peroxisomal pathways as emerging targets for intervention in age-related disease. Full article
(This article belongs to the Special Issue Understanding Aging Mechanisms to Prevent Age-Related Diseases: 2nd Edition)
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31 pages, 1151 KB  
Review
Aging and Corneal Nerve Health: Mechanisms of Degeneration and Emerging Therapies for the Cornea
by Hanieh Niktinat, Melinda Alviar, Marziyeh Kashani, Hamed Massoumi, Ali R. Djalilian and Elmira Jalilian
Cells 2025, 14(21), 1730; https://doi.org/10.3390/cells14211730 - 4 Nov 2025
Cited by 2 | Viewed by 2468
Abstract
Corneal nerves play a crucial role in maintaining ocular surface homeostasis by supporting the functional integrity of corneal epithelial, stromal, and endothelial cells; modulating tear secretion; and facilitating sensory responses essential for overall ocular health. With advancing age, these highly specialized peripheral sensory [...] Read more.
Corneal nerves play a crucial role in maintaining ocular surface homeostasis by supporting the functional integrity of corneal epithelial, stromal, and endothelial cells; modulating tear secretion; and facilitating sensory responses essential for overall ocular health. With advancing age, these highly specialized peripheral sensory fibers undergo progressive attrition and morphologic distortion driven by the canonical hallmarks of aging including genomic instability, impaired proteostasis, mitochondrial dysfunction, and chronic low-grade inflammation. The resulting neuro-immune dysregulation reduces trophic support, delays wound healing, and predisposes older adults to dry-eye disease, neurotrophic keratopathy, and postsurgical hypoesthesia. Age-exacerbating cofactors including diabetes, dyslipidemia, neurodegenerative disorders, topical preservatives, chronic contact-lens wear, herpes zoster ophthalmicus, and ocular-surface hypoxia further accelerate sub-basal nerve rarefaction and functional decline. This review provides an overview of age-related physiological alterations in ocular surface nerves, with a particular emphasis on corneal innervation. It also discusses risk factors that speed up these changes. Given the inherently limited regenerative capacity of corneal nerves and their inability to fully restore to baseline conditions following injury or degeneration, it is critical to identify and develop effective strategies aimed at mitigating or delaying physiological nerve degeneration and promoting nerve regeneration. This review also brings up emerging therapeutic strategies, including regenerative medicine, neuroprotective agents, and lifestyle interventions aimed at mitigating age-related corneal nerve degeneration. Full article
(This article belongs to the Special Issue Understanding Aging Mechanisms to Prevent Age-Related Diseases: 2nd Edition)
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22 pages, 925 KB  
Review
The Emerging Role of Water Loss in Dog Aging
by Gabriella Guelfi, Camilla Capaccia, Vicente Francisco Ratto, Antonello Bufalari, Leonardo Leonardi, Luca Mechelli, Simone Cenci and Margherita Maranesi
Cells 2025, 14(7), 545; https://doi.org/10.3390/cells14070545 - 4 Apr 2025
Cited by 3 | Viewed by 3372
Abstract
Aging involves progressive physiological changes, including the dysregulation of water homeostasis, essential for cellular function, neuronal signaling, and musculoskeletal integrity. This review explores the emerging role of water loss as a central and underestimated driver of functional decline in aging, with a focus [...] Read more.
Aging involves progressive physiological changes, including the dysregulation of water homeostasis, essential for cellular function, neuronal signaling, and musculoskeletal integrity. This review explores the emerging role of water loss as a central and underestimated driver of functional decline in aging, with a focus on the dog, both as a clinically relevant target species and as a model for human aging. Age-related alterations in water metabolism—driven by changes in body composition, aquaporin (AQP) expression, electrolyte imbalances, reduced thirst perception, and impaired urine concentration—lead to intracellular and extracellular dehydration, exacerbating functional decline. We examine molecular mechanisms of water regulation involving AQPs and osmolytes, and describe how dehydration contributes to structural and metabolic dysfunction across key biological compartments, including the kidney, brain, bone, and skeletal muscle. Physiological dehydration, a hallmark of aging, intensifies inflammaging, accelerating tissue degeneration. In particular, we highlight how water loss impairs solvent capacity, solute transport, protein conformation, and cellular communication. Despite the known role of macronutrients in geriatric nutrition, hydration remains an often-overlooked factor in aging management. We argue for its inclusion as a fourth pillar in the nutritional approach to veterinary geriatrics, alongside protein, fat, and fiber. By investigating aging-associated water loss in dogs—species that share environments and lifestyle patterns with humans—we propose hydration-centered strategies to promote healthy aging in both veterinary and comparative medicine. Full article
(This article belongs to the Special Issue Understanding Aging Mechanisms to Prevent Age-Related Diseases: 2nd Edition)
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