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Biomedicines
Special Issues
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: 31 May 2025 | Viewed by 4460

Special Issue Editor

Dr. David J. Rademacher

E-Mail Website
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

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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • 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
Viewed by 994
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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Figure 1

Figure 1
<p>The intracellular stages of gap junction formation. The connexins are synthesized as monomers in the endoplasmic reticulum, then transported to the Goldgi apparatus, where they assemble into hexameric structures, connexons, which are then exported to the cell membrane, forming a hemichannel. The connexons of the neighboring cells form an intercellular channel of gap junctions by connecting with each other.</p> Full article ">Figure 2
<p>The regulation of gap junction operation. The opening and closing of gap junctions are regulated by extracellular and intracellular factors such as pH, calcium ion concentration, and connexin phosphorylation. Gap junctions serve to move ions and small molecules up to 1.2 kDa between adjacent cells. The cells can exchange molecules through gap junctions such as carbohydrates, nucleotides, second messengers (cAMP or cGMP), small peptides, and RNA.</p> Full article ">Figure 3
<p>Intracellular localization and intercellular functioning of connexins. Abbreviation: AG—Apparatus of Goldgi, N—Nucleus, ER—Endoplasmic Reticulum, GJ—Gap Junction Channel, PM—Plasma Membrane.</p> Full article ">
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
Cited by 2 | Viewed by 2516
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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Figure 1

Figure 1
<p>Cellular senescence contributes to the aging of bone tissue and the onset of osteoporosis. In osteoporosis, senescent osteocytes release various senescence-associated secretory phenotype (SASPs), such as interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-1 beta (IL-1β), tumor necrosis factor α (TNF-α), monocyte chemoattractant protein-1 (MCP-1), matrix metalloproteinase-3 (MMP-3), and matrix metalloproteinase-13 (MMP-13). These alter bone turnover, reducing bone formation by osteoblasts, increasing bone resorption by osteoclasts, and promoting the progression of osteoporosis.</p> Full article ">Figure 2
<p>Cellular senescence contributes to the aging of muscle tissue and the onset of sarcopenia. Cellular senescence in sarcopenia is a process in which specific senescence markers, such as p16, p21, and p53, block the cell cycle by inhibiting the growth and proliferation of satellite cells. In turn, senescent satellite cells release various senescence-associated secretory phenotypes (SASPs), such as endothelin-1 (ET-1), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor α (TNF-α), matrix metalloproteinase-3 (MMP-3), and forkhead box O1 (FoxO1). In muscle tissue, SASPs increase (up arrow) oxidative stress, inflammation, and apoptosis and reduce (down arrow) myogenic potential. Consequently, muscle atrophy increases, and muscle strength decreases, promoting the onset of sarcopenia.</p> Full article ">Figure 3
<p>Cellular senescence contributes to cartilage tissue aging and the onset of osteoarthritis. Cellular senescence in osteoarthritis is induced by specific senescence markers, such as p16, p21, and p53, which block the cell cycle and inhibit chondrocyte growth and proliferation. In turn, senescent chondrocytes release various senescence-associated secretory phenotypes (SASPs), such as interleukin-1 (IL-1), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor α (TNF-α), matrix metalloproteinase-3 (MMP-3), and matrix metalloproteinase-13 (MMP-13). These factors increase (up arrow) inflammation, joint pain, and mitochondrial dysfunction while reducing (down arrow) autophagy by promoting the onset of osteoarthritis.</p> Full article ">Figure 4
<p>Anti-senescence strategies to counteract osteoporosis, sarcopenia, and osteoarthritis. The main strategies to counteract cellular senescence characterizing age-related musculoskeletal disorders include exercise, such as running, jumping, and weightlifting, and nutrition, rich in vitamin D, blueberries, resveratrol, curcumin, or based on calorie restriction. The use of senolytics and senomorphs, such as flavonoids, quercetin, and metformin, is also a useful tool to counteract senescent cell accumulation. Overall, these strategies promote tissue homeostasis by reducing (down arrow) the levels of p16, p21, tumor necrosis factor α (TNF-α), mammalian target of rapamycin (mTOR), and insulin-like growth factor-1 (IGF-1), as well as increasing (up arrow) the expression of sirtuin 1 (Sirt1), sirtuin 3 (Sirt3), irisin, and β-aminoisobutyric acid (BAIBA). Consequently, an increase in bone formation, joint function, muscle regeneration, and mitochondrial function has been observed in association with a reduction in inflammation, counteracting the onset and/or progression of osteoporosis, sarcopenia, and osteoarthritis.</p> Full article ">
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