Cellular Senescence in Age-Related Diseases: Pathophysiology and Therapeutic Approaches

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 May 2025 | Viewed by 2724

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Stritch School of Medicine, Core Microscopy Facility and Department of Microbiology and Immunology, Loyola University Chicago, Chicago, IL USA
Interests: neurodegenerative disease; addiction; microscopy; senescence; therapeutics
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Special Issue Information

Dear Colleagues,

Cellular senescence, discovered in the 1960s, is a homeostatic response triggered by aging-associated insults, such as genomic instability and telomere attrition. It is characterized by a stable cell cycle arrest, which prevents the proliferation of damaged cells, and profound phenotypic changes, such as the production of a complex mixture of biologically active secreted factors, referred to as the senescence-associated secretory phenotype (SASP). As cellular senescence, a central hallmark of aging, plays an important role in age-related diseases including diabetes, cardiovascular disease, cancer, and neurodegenerative diseases, interventions targeting senescence are potential therapies for these diseases. The finding of an increased life span in murine models after the removal of senescent cells underscored the utility of targeting senescence for therapeutic benefits. Several therapeutic approaches have been developed. These include the development of drugs that selectively eliminate senescent cells,  known as senolytics, the development of drugs that modulate the SASP, known as senomorphics, and the development of drugs that revert senescence to allow senescent cells to enter the cell cycle, known as senoreverters. This Special Issue welcomes articles that clarify the molecular and physiological properties of senescent cells, shed light on the role of cellular senescence in the pathophysiology of age-related diseases, or describe the development of novel therapeutic approaches targeting cellular senescence.

Dr. David J. Rademacher
Guest Editor

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Keywords

  • cellular senescence
  • senescence-associated secretory phenotype
  • aging
  • senolytics
  • senomorphics
  • senoreverters
  • therapeutics

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Published Papers (2 papers)

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Review

14 pages, 1015 KiB  
Review
Connexins and Aging-Associated Respiratory Disorders: The Role in Intercellular Communications
by Tatiana Zubareva, Ekaterina Mironova, Anna Panfilova, Yulia Krylova, Gianluigi Mazzoccoli, Maria Greta Pia Marasco, Igor Kvetnoy and Peter Yablonsky
Biomedicines 2024, 12(11), 2599; https://doi.org/10.3390/biomedicines12112599 - 13 Nov 2024
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Abstract
This article reviews the contemporary understanding of the functional role of connexins in intercellular communications, their involvement in maintaining cellular and tissue homeostasis, and in aging-associated respiratory disease pathogenesis. Connexins are discussed as potential therapeutic targets. The review particularly focuses on the involvement [...] Read more.
This article reviews the contemporary understanding of the functional role of connexins in intercellular communications, their involvement in maintaining cellular and tissue homeostasis, and in aging-associated respiratory disease pathogenesis. Connexins are discussed as potential therapeutic targets. The review particularly focuses on the involvement of gap junction connexins and hemichannels in the transfer of calcium ions, metabolite molecules, ATP, and mitochondria through the cell membrane. Various disorders in the regulation of intercellular communication can heavily contribute to the pathogenesis of multiple diseases, including respiratory system diseases. A deeper understanding of molecular mechanisms underlying the activities of various connexins in gap junction channels will enable the prospective development of therapeutic approaches by either inhibiting or stimulating the activities of a certain connexin, while considering its critical functions in intercellular communications on the whole. Full article
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17 pages, 3186 KiB  
Review
Cellular Senescence: The Driving Force of Musculoskeletal Diseases
by Angela Falvino, Beatrice Gasperini, Ida Cariati, Roberto Bonanni, Angela Chiavoghilefu, Elena Gasbarra, Annalisa Botta, Virginia Tancredi and Umberto Tarantino
Biomedicines 2024, 12(9), 1948; https://doi.org/10.3390/biomedicines12091948 - 26 Aug 2024
Viewed by 1377
Abstract
The aging of the world population is closely associated with an increased prevalence of musculoskeletal disorders, such as osteoporosis, sarcopenia, and osteoarthritis, due to common genetic, endocrine, and mechanical risk factors. These conditions are characterized by degeneration of bone, muscle, and cartilage tissue, [...] Read more.
The aging of the world population is closely associated with an increased prevalence of musculoskeletal disorders, such as osteoporosis, sarcopenia, and osteoarthritis, due to common genetic, endocrine, and mechanical risk factors. These conditions are characterized by degeneration of bone, muscle, and cartilage tissue, resulting in an increased risk of fractures and reduced mobility. Importantly, a crucial role in the pathophysiology of these diseases has been proposed for cellular senescence, a state of irreversible cell cycle arrest induced by factors such as DNA damage, telomere shortening, and mitochondrial dysfunction. In addition, senescent cells secrete pro-inflammatory molecules, called senescence-associated secretory phenotype (SASP), which can alter tissue homeostasis and promote disease progression. Undoubtedly, targeting senescent cells and their secretory profiles could promote the development of integrated strategies, including regular exercise and a balanced diet or the use of senolytics and senomorphs, to improve the quality of life of the aging population. Therefore, our review aimed to highlight the role of cellular senescence in age-related musculoskeletal diseases, summarizing the main underlying mechanisms and potential anti-senescence strategies for the treatment of osteoporosis, sarcopenia, and osteoarthritis. Full article
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