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 1141

Special Issue Editors


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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
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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

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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

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Keywords

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

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Published Papers (1 paper)

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Research

13 pages, 1831 KiB  
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 695
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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