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Biology
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Cellular Senescence in Health and Disease
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Cellular Senescence in Health and Disease

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Cell Biology".

Deadline for manuscript submissions: closed (1 February 2024) | Viewed by 13645

Special Issue Editors

Dr. Ming Xu

E-Mail Website
Guest Editor
UConn Center on Aging, UConn Health, Farmington, CT 06030, USA
Interests: aging; cellular senescence; frailty; diabetes; geroscience; bone metabolism; single-cell transcriptomics
Dr. Xu Zhang

E-Mail Website
Guest Editor
1. Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN 55905, USA
2. Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, MN 55905, USA
Interests: aging; cellular senescence; skeletal muscle; age-related diseases; single-cell multi-omics; live cell imaging

Special Issue Information

Dear Colleagues,

Emerging evidence indicates that cellular senescence plays an important role in a wide range of pathological and physiological conditions. Cellular senescence represents a distinct cell fate characterized by replicative arrest in response to a host of extrinsic and intrinsic stresses. Targeting senescent cells have been shown to alleviate many diseases and might represent a promising pharmacological target for alleviating effects of fundamental aging processes.

In this Special Issue, we are pleased to invite you to submit your studies to help us to further understand cellular senescence. This Special Issue aims to provide a platform to publish a number of studies relevant to cellular senescence in a smooth and timely manner. Original research articles, reviews, and brief reports are welcome.

Research areas may include (but are not limited to) the following:

  1. the role of senescent cells in diseases;
  2. the heterogeneity of senescent cells;
  3. the mechanistic regulations of cellular senescence;
  4. “omics” datasets;
  5. human studies.

Early-stage junior faculty members are especially encouraged.

We look forward to receiving your contributions.

Dr. Ming Xu
Dr. Xu Zhang
Guest Editors

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. Biology 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 2700 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

  • aging
  • morbidity
  • cellular senescence
  • geroscience
  • inflammation
  • heterogeneity

Published Papers (6 papers)

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Research

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13 pages, 1311 KiB  
Article
BLTR1 Is Decreased in Steroid Resistant Pro-Inflammatory CD28nullCD8+ T Lymphocytes in Patients with COPD—The Spillover Hypothesis Explained?
by Greg Hodge, Hubertus Jersmann, Mark Holmes, Patrick Asare, Eugene Roscioli, Paul N. Reynolds and Sandra Hodge
Biology 2023, 12(9), 1261; https://doi.org/10.3390/biology12091261 - 20 Sep 2023
Viewed by 835
Abstract
Introduction: Pro-inflammatory CD8+ T cells are increased in the lungs and also in the peripheral circulation of both smokers and chronic obstructive pulmonary disease (COPD) patients. The reason for this is unclear but has been described as a spillover from cells in the [...] Read more.
Introduction: Pro-inflammatory CD8+ T cells are increased in the lungs and also in the peripheral circulation of both smokers and chronic obstructive pulmonary disease (COPD) patients. The reason for this is unclear but has been described as a spillover from cells in the lungs that may cause the systemic inflammation noted in COPD. We have recently shown an increase in steroid-resistant CD28nullCD8+ senescent lymphocytes in the lungs and peripheral blood in COPD. Leukotreine B4 (LB4) receptor 1 (BLTR1) is involved in recruitment of CD8+ T cells to sites of inflammation, and we hypothesized that it may be involved in the migration of these senescent lymphocytes from the lungs in COPD. Methods: Via flow cytometry and Western blot BLTR1, IFNγ, and TNFα expression were measured in peripheral blood, BAL, and large proximal and small distal airway CD28±, CD8± T, and NKT-like cells from COPD patients and healthy control subjects (±prednisolone) following in vitro stimulation. Chemotaxis of leucocyte subsets was determined (±LB4 ± prednisolone). Results: There was an increase in BLTR1-CD28nullCD8+ lymphocytes in the lungs and blood in patients with COPD compared with controls. BLTR1-CD28nullCD8+ T and NKT-like cells produce more IFN/TNF than BLTR+ cells and fail to migrate to LTB4. Treatment with 1 µM prednisolone in vitro resulted in upregulation of BLTR1 expression in pro-inflammatory CD28nullCD8+ cells and migration to LB4. Conclusions: Loss of BLTR1 is associated with an increased inflammatory potential of CD28nullCD8+ T cells and may allow these pro-inflammatory steroid-resistant cells to migrate to peripheral blood. Treatment strategies that upregulate BLTR1 may reduce systemic inflammation and associated co-morbidity in patients with COPD. Full article
(This article belongs to the Special Issue Cellular Senescence in Health and Disease)
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20 pages, 10564 KiB  
Article
Epimorphic Regeneration of Elastic Cartilage: Morphological Study into the Role of Cellular Senescence
by Yana Valieva, Aleksandra Igrunkova, Alexey Fayzullin, Natalia Serejnikova, Aleksandr Kurkov, Nafisa Fayzullina, Dina Valishina, Alesia Bakulina, Peter Timashev and Anatoly Shekhter
Biology 2023, 12(4), 565; https://doi.org/10.3390/biology12040565 - 07 Apr 2023
Viewed by 1702
Abstract
Control over endogenous reparative mechanisms is the future of regenerative medicine. The rabbit ear defect is a rare model which allows the observation of the epimorphic regeneration of elastic cartilage. However, the mechanisms of phenotypical restoration of this highly differentiated tissue have not [...] Read more.
Control over endogenous reparative mechanisms is the future of regenerative medicine. The rabbit ear defect is a rare model which allows the observation of the epimorphic regeneration of elastic cartilage. However, the mechanisms of phenotypical restoration of this highly differentiated tissue have not been studied. We modelled circular ear defects of different sizes (4, 6, and 8 mm in diameter) in 12 laboratory rabbits, and observed them during 30, 60, 90, and 120 day periods. Excised tissues were processed and analyzed by standard histological methods and special histochemical reactions for senescence associated-β-galactosidase and lectin markers. We demonstrated that larger defects caused significant elevation of senescence associated-β-galactosidase in chondrocytes. The fullness of epimorphic regeneration of elastic cartilage depended on the activation of cellular senescence and synthesis of elastic fibers. Further investigation into the role of cells with senescence-associated secretory phenotype in damaged tissues can present new targets for controlled tissue regeneration. Full article
(This article belongs to the Special Issue Cellular Senescence in Health and Disease)
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Review

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27 pages, 1517 KiB  
Review
Translating Senotherapeutic Interventions into the Clinic with Emerging Proteomic Technologies
by Amit K. Dey, Reema Banarjee, Mozhgan Boroumand, Delaney V. Rutherford, Quinn Strassheim, Thedoe Nyunt, Bradley Olinger and Nathan Basisty
Biology 2023, 12(10), 1301; https://doi.org/10.3390/biology12101301 - 02 Oct 2023
Viewed by 2931
Abstract
Cellular senescence is a state of irreversible growth arrest with profound phenotypic changes, including the senescence-associated secretory phenotype (SASP). Senescent cell accumulation contributes to aging and many pathologies including chronic inflammation, type 2 diabetes, cancer, and neurodegeneration. Targeted removal of senescent cells in [...] Read more.
Cellular senescence is a state of irreversible growth arrest with profound phenotypic changes, including the senescence-associated secretory phenotype (SASP). Senescent cell accumulation contributes to aging and many pathologies including chronic inflammation, type 2 diabetes, cancer, and neurodegeneration. Targeted removal of senescent cells in preclinical models promotes health and longevity, suggesting that the selective elimination of senescent cells is a promising therapeutic approach for mitigating a myriad of age-related pathologies in humans. However, moving senescence-targeting drugs (senotherapeutics) into the clinic will require therapeutic targets and biomarkers, fueled by an improved understanding of the complex and dynamic biology of senescent cell populations and their molecular profiles, as well as the mechanisms underlying the emergence and maintenance of senescence cells and the SASP. Advances in mass spectrometry-based proteomic technologies and workflows have the potential to address these needs. Here, we review the state of translational senescence research and how proteomic approaches have added to our knowledge of senescence biology to date. Further, we lay out a roadmap from fundamental biological discovery to the clinical translation of senotherapeutic approaches through the development and application of emerging proteomic technologies, including targeted and untargeted proteomic approaches, bottom-up and top-down methods, stability proteomics, and surfaceomics. These technologies are integral for probing the cellular composition and dynamics of senescent cells and, ultimately, the development of senotype-specific biomarkers and senotherapeutics (senolytics and senomorphics). This review aims to highlight emerging areas and applications of proteomics that will aid in exploring new senescent cell biology and the future translation of senotherapeutics. Full article
(This article belongs to the Special Issue Cellular Senescence in Health and Disease)
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19 pages, 1654 KiB  
Review
Interaction between Autophagy and Senescence in Pancreatic Beta Cells
by Francesko Hela and Cristina Aguayo-Mazzucato
Biology 2023, 12(9), 1205; https://doi.org/10.3390/biology12091205 - 04 Sep 2023
Viewed by 1485
Abstract
Aging leads to an increase in cellular stress due to the fragility of the organism and the inability to cope with it. In this setting, there is a higher chance of developing different cardiometabolic diseases like diabetes. Cellular senescence and autophagy, both hallmarks [...] Read more.
Aging leads to an increase in cellular stress due to the fragility of the organism and the inability to cope with it. In this setting, there is a higher chance of developing different cardiometabolic diseases like diabetes. Cellular senescence and autophagy, both hallmarks of aging and stress-coping mechanisms, have gained increased attention for their role in the pathophysiology of diabetes. Studies show that impairing senescence dampens and even prevents diabetes while the role of autophagy is more contradictory, implying a context- and disease-stage-dependent effect. Reports show conflicting data about the effect of autophagy on senescence while the knowledge about this interaction in beta cells remains scarce. Elucidating this interaction between autophagy and senescence in pancreatic beta cells will lead to an identification of their respective roles and the extent of the effect each mechanism has on beta cells and open new horizons for developing novel therapeutic agents. To help illuminate this relationship we will review the latest findings of cellular senescence and autophagy with a special emphasis on pancreatic beta cells and diabetes. Full article
(This article belongs to the Special Issue Cellular Senescence in Health and Disease)
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14 pages, 1809 KiB  
Review
Role of Senescent Cells in Cutaneous Wound Healing
by Allison M. Andrade, Mingda Sun, Nathan S. Gasek, Geneva R. Hargis, Roshanak Sharafieh and Ming Xu
Biology 2022, 11(12), 1731; https://doi.org/10.3390/biology11121731 - 29 Nov 2022
Cited by 6 | Viewed by 3016
Abstract
Cellular senescence has gained increasing attention in the field of aging research. Senescent cells have been implicated in biological aging processes, tumorigenesis, development, and wound repair amongst other processes and pathologies. Recent findings reveal that senescent cells can both promote and inhibit cutaneous [...] Read more.
Cellular senescence has gained increasing attention in the field of aging research. Senescent cells have been implicated in biological aging processes, tumorigenesis, development, and wound repair amongst other processes and pathologies. Recent findings reveal that senescent cells can both promote and inhibit cutaneous wound healing processes. Relating senescent cells in acute and chronic wounds will help to clarify their role in wound healing processes and inform our understanding of senescent cell heterogeneity. To clarify this apparent contradiction and guide future research and therapeutic development, we will review the rapidly growing field of cellular senescence and its role in wound healing biology. Full article
(This article belongs to the Special Issue Cellular Senescence in Health and Disease)
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13 pages, 1055 KiB  
Review
Cellular Senescence and Periodontitis: Mechanisms and Therapeutics
by Sijia Chen, Dian Zhou, Ousheng Liu, Huan Chen, Yuehong Wang and Yueying Zhou
Biology 2022, 11(10), 1419; https://doi.org/10.3390/biology11101419 - 29 Sep 2022
Cited by 5 | Viewed by 2763
Abstract
Periodontitis is a chronic inflammatory disease which increases in prevalence and severity in the older population. Aging is a leading risk factor for periodontitis, which exacerbates alveolar bone loss and results in tooth loss in the elderly. However, the mechanism by which aging [...] Read more.
Periodontitis is a chronic inflammatory disease which increases in prevalence and severity in the older population. Aging is a leading risk factor for periodontitis, which exacerbates alveolar bone loss and results in tooth loss in the elderly. However, the mechanism by which aging affects periodontitis is not well understood. There is considerable evidence to suggest that targeting cellular senescence could slow down the fundamental aging process, and thus alleviate a series of age-related pathological conditions, likely including alveolar bone loss. Recently, it has been discovered that the senescent cells accumulate in the alveolar bone and promote a senescence-associated secretory phenotype (SASP). Senescent cells interacting with bacteria, together with secreted SASP components altering the local microenvironment and inducing paracrine effects in neighboring cells, exacerbate the chronic inflammation in periodontal tissue and lead to more alveolar bone loss. This review will probe into mechanisms underlying excessive alveolar bone loss in periodontitis with aging and discuss potential therapeutics for the treatment of alveolar bone loss targeting cellular senescence and the SASP. Inspecting the relationship between cellular senescence and periodontitis will lead to new avenues of research in this field and contribute to developing potential translatable clinical interventions to mitigate or even reverse the harmful effects of aging on oral health. Full article
(This article belongs to the Special Issue Cellular Senescence in Health and Disease)
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