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Biomedicines
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Cellular Senescence in Age-Related Diseases: Pathophysiology and Therapeutic Approaches
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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: closed (31 December 2025) | Viewed by 18647

Editor

Dr. David J. Rademacher

E-Mail
Guest Editor
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
Special Issues, Collections and Topics in MDPI journals

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 (5 papers)

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Review

26 pages, 461 KB  
Review
Cellular Senescence in Neurodegeneration: From Cell Types to Therapeutic Opportunities
by Marta Zawadzka, Julia Rydzek, Julia Lizon, Zuzanna Krupa, Joanna Wrona and Sławomir Woźniak
Biomedicines 2026, 14(4), 758; https://doi.org/10.3390/biomedicines14040758 - 26 Mar 2026
Cited by 1 | Viewed by 1507
Abstract
Neurodegenerative diseases of the central nervous system, such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis, represent a growing health challenge in ageing populations. Among the mechanisms underlying these disorders, increasing attention has been directed toward the role of cellular senescence. This process, [...] Read more.
Neurodegenerative diseases of the central nervous system, such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis, represent a growing health challenge in ageing populations. Among the mechanisms underlying these disorders, increasing attention has been directed toward the role of cellular senescence. This process, triggered by chronic cellular and oxidative stress as well as DNA damage, leads to irreversible cell-cycle arrest and the development of the senescence-associated secretory phenotype (SASP). Within the central nervous system, the accumulation of senescent cells induces chronic inflammation, blood–brain barrier disruption, and progression of neurodegenerative processes. In this review, we present current evidence regarding the mechanisms of cellular senescence in the central nervous system, with particular emphasis on the role of SASP in neuroinflammation, vascular dysfunction, and neural tissue damage. Experimental and clinical data supporting the involvement of cellular senescence in the pathogenesis of Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis are discussed. The review also covers methods for identifying senescent cells in the brain, including molecular marker-based approaches and machine learning-based tools. Importantly, we discuss the methodological limitations of commonly used senescence markers, such as their limited specificity and the risk of false-positive detection, particularly in the heterogeneous cellular environment of the central nervous system. Strategies to improve detection reliability discussed in this review include the use of multimarker signatures, analysis of SASP components using qRT-PCR and ELISA, as well as transcriptomic approaches such as RNA sequencing and single-cell RNA sequencing. Furthermore, we analyze therapeutic strategies targeting senescent cells—senolytics, senomorphics, and SASP modulation—together with their limitations and associated clinical challenges. The collected evidence indicates that precise characterization of senescent cell populations in the brain is essential for the development of disease-modifying therapies for neurodegenerative disorders. Full article
(This article belongs to the Special Issue Cellular Senescence in Age-Related Diseases: Pathophysiology and Therapeutic Approaches)
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16 pages, 310 KB  
Review
The Role of Cellular Senescence and SASP in the Pathogenesis of Atherosclerosis and the Therapeutic Potential of Senolytic Strategies in Cardiovascular Diseases
by Zuzanna Krupa, Joanna Wrona, Marta Zawadzka, Julia Rydzek, Julia Lizon, Paulina Kalemba, Konrad Kochman, Paweł Iwaszkiewicz, Robert Iwanowski and Sławomir Woźniak
Biomedicines 2026, 14(2), 331; https://doi.org/10.3390/biomedicines14020331 - 31 Jan 2026
Cited by 9 | Viewed by 2082
Abstract
Cellular senescence is a permanent cell cycle arrest that plays a critical role in the development and pathogenesis of age-related diseases. This paper aims to present the biological mechanisms of cellular senescence and the role of the senescence-associated secretory phenotype (SASP) in the [...] Read more.
Cellular senescence is a permanent cell cycle arrest that plays a critical role in the development and pathogenesis of age-related diseases. This paper aims to present the biological mechanisms of cellular senescence and the role of the senescence-associated secretory phenotype (SASP) in the pathogenesis of atherosclerosis, as well as to discuss therapeutic strategies targeting senescent cells in cardiovascular diseases. Different types of cellular senescence are described, including replicative, stress-induced, and oncogene-induced senescence, along with the composition and regulation of SASP and its impact on chronic inflammation, endothelial dysfunction, vascular remodeling, and plaque destabilization. The involvement of senescent endothelial cells, vascular smooth muscle cells, and macrophages in the initiation and progression of atherosclerosis is also discussed. The paper reviews current research on senolytic and senomorphic therapies and highlights emerging approaches such as immunosenolytic and epigenetic interventions. The therapeutic potential of these strategies in reducing chronic vascular inflammation and improving plaque stability, as well as their limitations and challenges in clinical application, is emphasized. Full article
(This article belongs to the Special Issue Cellular Senescence in Age-Related Diseases: Pathophysiology and Therapeutic Approaches)
34 pages, 1138 KB  
Review
Role of Cellular Senescence in Parkinson’s Disease: Potential for Disease-Modification Through Senotherapy
by David J. Rademacher, Jacob E. Exline and Eileen M. Foecking
Biomedicines 2025, 13(6), 1400; https://doi.org/10.3390/biomedicines13061400 - 7 Jun 2025
Cited by 6 | Viewed by 5038
Abstract
Parkinson’s disease (PD) is an aging-related neurodegenerative disease characterized by a progressive loss of dopamine (DA)-secreting neurons in the substantia nigra. Most of the currently available treatments attempt to alleviate the disease symptoms by increasing DA transmission in the brain and are associated [...] Read more.
Parkinson’s disease (PD) is an aging-related neurodegenerative disease characterized by a progressive loss of dopamine (DA)-secreting neurons in the substantia nigra. Most of the currently available treatments attempt to alleviate the disease symptoms by increasing DA transmission in the brain and are associated with unpleasant side effects. Since there are no treatments that modify the course of PD or regenerate DA neurons, identifying therapeutic strategies that slow, stop, or reverse cell death in PD is of critical importance. Here, factors that confer vulnerability of substantia nigra DA neurons to cell death and the primary mechanisms of PD pathogenesis, including cellular senescence, a cellular stress response that elicits a stable cell cycle arrest in mitotic cells and profound phenotypic changes including the implementation of a pro-inflammatory secretome, are reviewed. Additionally, a discussion of the characteristics, mechanisms, and markers of cellular senescence and the development of approaches to target senescent cells, referred to as senotherapeutics, is included. Although the senotherapeutics curcumin, fisetin, GSK-650394, and astragaloside IV had disease-modifying effects in in vitro and in vivo models of PD, the potential long-term side effects of these compounds remain unclear. It remains to be elucidated whether their beneficial effects will translate to non-human primate models and/or human PD patients. The enhanced selectivity, safety, and/or efficacy of next generation senotherapeutic strategies including senolytic peptides, senoreverters, proteolysis-targeting chimeras, pro-drugs, immunotherapy, and nanoparticles will also be reviewed. Although these next generation senotherapeutics may have advantages, none have been tried in models of PD. Full article
(This article belongs to the Special Issue Cellular Senescence in Age-Related Diseases: Pathophysiology and Therapeutic Approaches)
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14 pages, 1015 KB  
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
Cited by 2 | Viewed by 2493
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
(This article belongs to the Special Issue Cellular Senescence in Age-Related Diseases: Pathophysiology and Therapeutic Approaches)
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17 pages, 3186 KB  
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
Cited by 24 | Viewed by 5716
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
(This article belongs to the Special Issue Cellular Senescence in Age-Related Diseases: Pathophysiology and Therapeutic Approaches)
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