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Inflammation and Cellular Senescence in Age-Related Diseases

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: 20 May 2025 | Viewed by 1862

Special Issue Editors


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Guest Editor
Laboratory of Immunopathology and Immunosenescence, Department of Biomedicine, Neuroscience and Advanced Diagnostics, University of Palermo, 90134 Palermo, Italy
Interests: ageing; age-related diseases; centenarians; immunogenetics; immunosenescence; inflammation; longevity; successful ageing; unsuccessful ageing
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Laboratory of Immunopathology and Immunosenescence, Department of Biomedicine, Neuroscience and Advanced Diagnostics, University of Palermo, Palermo, Italy
Interests: autoimmunity; immune response; immunogenetics; immunosenescence; inflammaging; immunopathology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

As is well known, life expectancy has increased worldwide. Unfortunately, this increase in lifespan is not accompanied in most older individuals by an increase in healthy life expectancy, the so-called health-span. The main cause of this disability is the onset of ageing-related diseases (ARDs), and it is time to seriously address how to prevent or at least postpone the appearance of these debilitating diseases. Ageing in good health would result in a net gain for society in social, economic, and health terms. The purpose of this Special Issue is to expand our knowledge in the fields of ARDs. Its ambition is to publish articles that explore the multiple factors responsible for the etiopathogenesis and pathophysiology of these diseases, with the aim of better prevention or treatment (and a particular focus on the role of inflammatory processes and cellular senescence). Contributions may come from all basic and applied disciplines that research these processes. Naturally, the role of the exposome in determining these diseases may also be analyzed, as well as possible preventive interventions. By disseminating research on these topics, conducted either on humans or models, this Special Issue aims to create interdisciplinary connections, thereby facilitating a comprehensive understanding of ARDs, and hence of their prevention.

Prof. Dr. Calogero Caruso
Prof. Dr. Giuseppina Candore
Guest Editors

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Keywords

  • age-related diseases
  • exposome
  • prevention
  • pathophysiology
  • pathogenesis
  • inflammation
  • senescence

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Published Papers (1 paper)

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Research

23 pages, 20158 KiB  
Article
Inflammation and Fibrosis in Progeria: Organ-Specific Responses in an HGPS Mouse Model
by Peter Krüger, Moritz Schroll, Felix Fenzl, Eva-Maria Lederer, Ramona Hartinger, Rouven Arnold, Deniz Cagla Togan, Runjia Guo, Shiyu Liu, Andreas Petry, Agnes Görlach and Karima Djabali
Int. J. Mol. Sci. 2024, 25(17), 9323; https://doi.org/10.3390/ijms25179323 - 28 Aug 2024
Viewed by 1588
Abstract
Hutchinson–Gilford Progeria Syndrome (HGPS) is an extremely rare genetic disorder that causes accelerated aging, due to a pathogenic variant in the LMNA gene. This pathogenic results in the production of progerin, a defective protein that disrupts the nuclear lamina’s structure. In our study, [...] Read more.
Hutchinson–Gilford Progeria Syndrome (HGPS) is an extremely rare genetic disorder that causes accelerated aging, due to a pathogenic variant in the LMNA gene. This pathogenic results in the production of progerin, a defective protein that disrupts the nuclear lamina’s structure. In our study, we conducted a histopathological analysis of various organs in the LmnaG609G/G609G mouse model, which is commonly used to study HGPS. The objective of this study was to show that progerin accumulation drives systemic but organ-specific tissue damage and accelerated aging phenotypes. Our findings show significant fibrosis, inflammation, and dysfunction in multiple organ systems, including the skin, cardiovascular system, muscles, lungs, liver, kidneys, spleen, thymus, and heart. Specifically, we observed severe vascular fibrosis, reduced muscle regeneration, lung tissue remodeling, depletion of fat in the liver, and disruptions in immune structures. These results underscore the systemic nature of the disease and suggest that chronic inflammation and fibrosis play crucial roles in the accelerated aging seen in HGPS. Additionally, our study highlights that each organ responds differently to the toxic effects of progerin, indicating that there are distinct mechanisms of tissue-specific damage. Full article
(This article belongs to the Special Issue Inflammation and Cellular Senescence in Age-Related Diseases)
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