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Cells
Special Issues
Experimental Systems to Model Aging Processes
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Experimental Systems to Model Aging Processes

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

Deadline for manuscript submissions: 20 October 2025 | Viewed by 2657

Special Issue Editors

Dr. Natascia Tiso

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Guest Editor
Developmental Genetics Laboratory, Department of Biology, University of Padova, via Ugo Bassi 58/B, I-35131 Padova, Italy
Interests: zebrafish models; aging research; inherited diseases; heart; mitochondria; endocrine; signaling pathway
Special Issues, Collections and Topics in MDPI journals
Dr. Giovanni Risato

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Guest Editor
1. Department of Biology, University of Padova, 35131 Padova, Italy
2. Department of Cardio-Thoraco-Vascular Sciences and Public Health, University of Padova, 35128 Padova, Italy
Interests: zebrafish; inherited diseases; cardiomyopathy; mitochondria; signaling pathway; drug testing
Dr. Ralf Dahm

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Guest Editor
Institute of Molecular Biology gGmbH (IMB), Ackermannweg 4, 55128 Mainz, Germany
Interests: ageing research; model organisms; effects of age-related diseases of the eye on visual perception and the work of artists; history of science; science communication

Special Issue Information

Dear Colleagues,

This Special Issue of Cells on "Experimental Systems to Model Aging Processes" aims to gather contributions from internationally leading aging researchers on model systems—ranging from traditional to emerging models—used to elucidate the mechanisms underlying aging. Contributions can be in the form of original scientific articles and reviews.

Aging is driven by a range of molecular and subcellular processes, which include genetic, epigenetic, and genomic alterations; the loss of proteostasis; dysregulated autophagy; metabolic dysfunctions; or the malfunction of cellular organelles. Additionally, aging is influenced by inter-cellular dynamics, including changes in signaling pathways, inflammatory processes, and microbial balance. These events, whether individually or interconnected, can be modeled in study systems both in vitro and in vivo, as well as ex vivo and in silico.

Elucidating these processes in experimental systems—from the most reductionist to the most complex—paves the way for identifying new molecular and cellular mechanisms, as well as potential targets to mitigate the negative outcomes associated with aging, including diseases such as cancer, osteoporosis, sarcopenia, diabetes, or neurodegenerative and cardiovascular diseases. This Special Issue welcomes contributions describing insights and approaches from all the above fields, as well as those summarizing recent advances and emerging developments. By publishing these, we hope to advance our understanding of the aging process and thereby aid the development of better strategies to prevent or mitigate negative aspects of aging, formulate targeted therapies for age-related diseases, and generally promote the well-being and healthy aging of the global population.

We look forward to your contributions.

Dr. Natascia Tiso
Dr. Giovanni Risato
Dr. Ralf Dahm
Guest Editors

Raquel Branas Casas
Guest Editor Assistant

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. 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
  • ageing
  • age-related
  • longevity
  • model
  • animal
  • signalling pathway
  • mechanism
  • in vitro
  • in vivo
  • cell culture
  • marker

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Published Papers (3 papers)

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Research

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16 pages, 2967 KB  
Article
Adeno-Associated Viral Gene Delivery of Wild-Type Human Tau Induces Progressive Hyperphosphorylation and Neuronal Cell Death in the Hippocampi of Middle-Aged Rats
by Ryan C. Gorzek, Aurelie Joly-Amado, Natalia Hurst-Calle, Graham L. Gabrielson, Maxine Miller, Sue Osting, Kevin R. Nash and Corinna Burger
Cells 2025, 14(16), 1238; https://doi.org/10.3390/cells14161238 - 11 Aug 2025
Viewed by 435
Abstract
Tau aggregation and the subsequent formation of neurofibrillary tangles are hallmarks of Alzheimer’s disease (AD) and other dementias. While accumulation of tau aggregates is believed to contribute to cell death and neurodegeneration, tau aggregation and hyperphosphorylation are also correlated with cognitive impairment in [...] Read more.
Tau aggregation and the subsequent formation of neurofibrillary tangles are hallmarks of Alzheimer’s disease (AD) and other dementias. While accumulation of tau aggregates is believed to contribute to cell death and neurodegeneration, tau aggregation and hyperphosphorylation are also correlated with cognitive impairment in AD. To understand the role of tau in neurodegeneration, we used adeno-associated virus serotype 9 (AAV9) to express human wild-type 4-repeat, 0-N-terminus tau isoform (AAV-htau) in the Cornu ammonis area 1 (CA1) region of the dorsal hippocampus of adult 6-month-old Fischer 344 rats. AAV expressing green fluorescent protein (AAV-GFP) or uninjected rats were used as controls. To characterize early phenotypes, we investigated pathological changes at 3, 8, and 12 weeks post-injection of AAV-htau. Our results show that at 3 weeks post-injection, there was already robust expression of human tau in the CA1 region of animals injected with AAV-htau compared to those injected with AAV-GFP or the uninjected controls. At 12 weeks post-injection, area CA1 showed a statistically significant reduction in cell number and a thinner neuronal layer all throughout the anterior dorsal hippocampus, as well as redistribution to the somatodendritic areas of CA1. We also found hyperphosphorylation of tau at all three timepoints. In spite of this pathology, we did not find any hippocampal-dependent cognitive impairment in rats overexpressing human tau. These results provide evidence of AAV-htau as a progressive model of tauopathy pathology to study changes in phosphorylation status and neuronal cell death that might precede cognitive impairment. Full article
(This article belongs to the Special Issue Experimental Systems to Model Aging Processes)
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13 pages, 1831 KB  
Article
Chloroquine Causes Aging-like Changes in Diaphragm Neuromuscular Junction Morphology in Mice
by Chloe I. Gulbronson, Sepideh Jahanian, Heather M. Gransee, Gary C. Sieck and Carlos B. Mantilla
Cells 2025, 14(6), 390; https://doi.org/10.3390/cells14060390 - 7 Mar 2025
Viewed by 1063
Abstract
Autophagy impairments have been implicated in various aging conditions. Previous studies in cervical motor neurons show an age-dependent increase in the key autophagy proteins LC3 and p62, reflecting autophagy impairment and autophagosome accumulation. Chloroquine is commonly used to inhibit autophagy by preventing autophagosome–lysosome [...] Read more.
Autophagy impairments have been implicated in various aging conditions. Previous studies in cervical motor neurons show an age-dependent increase in the key autophagy proteins LC3 and p62, reflecting autophagy impairment and autophagosome accumulation. Chloroquine is commonly used to inhibit autophagy by preventing autophagosome–lysosome fusion and may thus emulate the effects of aging on the neuromuscular system. Indeed, acute chloroquine administration in old mice decreases maximal transdiaphragmatic pressure generation, consistent with aging effects. We hypothesized that chloroquine alters diaphragm muscle neuromuscular junction (NMJ) morphology and increases denervation. Adult male and female C57BL/6 × 129J mice between 5 and 8 months of age were used to examine diaphragm muscle NMJ morphology and denervation following daily intraperitoneal injections of chloroquine (10 mg/kg/d) or vehicle for 7 days. The motor end-plates and pre-synaptic terminals were fluorescently labeled with α-bungarotoxin and anti-synaptophysin, respectively. Confocal microscopy was used to assess pre- and post-synaptic morphology and denervation. At diaphragm NMJs, chloroquine treatment decreased pre-synaptic volume by 12% compared to the vehicle (p < 0.05), with no change in post-synaptic volume. Chloroquine treatment increased the proportion of partially denervated NMJs by 2.7-fold compared to vehicle treatment (p < 0.05). The morphological changes observed were similar to those previously reported in the diaphragm muscles of 18-month-old mice. These findings highlight the importance of autophagy in the maintenance of the structural properties at adult NMJs in vivo. Full article
(This article belongs to the Special Issue Experimental Systems to Model Aging Processes)
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Review

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23 pages, 1044 KB  
Review
Cellular Models of Aging and Senescence
by Byunggik Kim, Dong I. Lee, Nathan Basisty and Dao-Fu Dai
Cells 2025, 14(16), 1278; https://doi.org/10.3390/cells14161278 - 18 Aug 2025
Viewed by 531
Abstract
Aging, a state of progressive decline in physiological function, is an important risk factor for chronic diseases, ranging from cancer and musculoskeletal frailty to cardiovascular and neurodegenerative diseases. Understanding its cellular basis is critical for developing interventions to extend human health span. This [...] Read more.
Aging, a state of progressive decline in physiological function, is an important risk factor for chronic diseases, ranging from cancer and musculoskeletal frailty to cardiovascular and neurodegenerative diseases. Understanding its cellular basis is critical for developing interventions to extend human health span. This review highlights the crucial role of in vitro models, discussing foundational discoveries like the Hayflick limit and the senescence-associated secretory phenotype (SASP), the utility of immortalized cell lines, and transformative human induced pluripotent stem cells (iPSCs) for aging and disease modeling and rejuvenation studies. We also examine methods to induce senescence and discuss the distinction between chronological time and biological clock, with examples of applying cells from progeroid syndromes and mitochondrial diseases to recapitulate some signaling mechanisms in aging. Although no in vitro model can perfectly recapitulate organismal aging, well-chosen models are invaluable for addressing specific mechanistic questions. We focus on experimental strategies to manipulate cellular aging: from “steering” cells toward resilience to “reversing” age-related phenotypes via senolytics, partial epigenetic reprogramming, and targeted modulation of proteostasis and mitochondrial health. This review ultimately underscores the value of in vitro systems for discovery and therapeutic testing while acknowledging the challenge of translating insights from cell studies into effective, organism-wide strategies to promote healthy aging. Full article
(This article belongs to the Special Issue Experimental Systems to Model Aging Processes)
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