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Biology
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Cellular Senescence in Development, Regeneration, Aging, and Cancer
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Cellular Senescence in Development, Regeneration, Aging, and Cancer

A special issue of Biology (ISSN 2079-7737).

Deadline for manuscript submissions: 31 December 2026 | Viewed by 2216

Special Issue Editor

Dr. Selim Chaib

E-Mail Website
Guest Editor
Cedars-Sinai Medical Center, Department of Medicine, 8687 Melrose Ave, Pacific Design Center, Office G-571, Los Angeles, CA 90069, USA
Interests: cellular senescence; aging; cancer; obesity; metabolism; geroscience; age-related diseases; inflammaging; senolytics

Special Issue Information

Dear Colleagues,

Cellular senescence is a phenomenon characterized by the cessation of cell division; it is a complex cell fate with significant implications for both cancer and aging. Cellular senescence serves as a critical tumor-suppressive mechanism by halting the proliferation of damaged cells but can also promote tumor progression and therapy resistance by creating a pro-tumorigenic microenvironment. Additionally, the accumulation of senescent cells during aging contributes to chronic diseases, as their pro-inflammatory secretome drives chronic inflammation, tissue dysfunction, and metabolic dysregulation, exacerbating age-related pathologies. Furthermore, recent studies have uncovered functional roles for senescence in embryonic development and regeneration.

In this Special Issue, original research articles and reviews are welcome to address the latest advances in understanding cellular senescence at the intersection of cancer and aging, as well as its roles in development and regeneration. Research areas may include (but are not limited to) the following: molecular mechanisms or markers of cellular senescence, the role of the immune system in senescent cell clearance and interaction, novel therapeutic strategies targeting senescence (senolytics and senomorphics), implications of cellular senescence in cancer and aging-related diseases, and roles of cell senescence in regeneration, development, and longevity across species.

By integrating insights from geroscience, cancer biology, regenerative medicine, developmental biology, and immunology, this Special Issue aims to highlight fundamental research and emerging translational strategies to target cellular senescence for extending healthspan and enhancing anti-cancer therapies and improve our understanding of the regenerative and developmental processes influenced by cellular senescence.

I look forward to receiving your contributions.

Dr. Selim Chaib
Guest Editor

Manuscript Submission Information

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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 semimonthly 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

  • cellular senescence
  • aging
  • cancer
  • obesity
  • metabolism
  • geroscience
  • age-related diseases
  • SASP
  • senolytics
  • biomarkers

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Published Papers (2 papers)

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15 pages, 3124 KB  
Article
Force-Dependent Presence of Senescent Cells Expressing Vascular Endothelial Growth Factor During Orthodontic Tooth Movement
by Yohei Morihana, Masato Nakagawa, Yue Zhou, Hidetoshi Morikuni, Zi Deng, Yoshitomo Honda and Aki Nishiura
Biology 2026, 15(2), 187; https://doi.org/10.3390/biology15020187 - 19 Jan 2026
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Abstract
Orthodontic force magnitude influences angiogenesis during orthodontic tooth movement (OTM); however, the role of senescent cells remains largely unclear. This study investigated the localization of senescent cells and their expression of vascular endothelial growth factor (VEGF) during angiogenesis using a rat horizontal OTM [...] Read more.
Orthodontic force magnitude influences angiogenesis during orthodontic tooth movement (OTM); however, the role of senescent cells remains largely unclear. This study investigated the localization of senescent cells and their expression of vascular endothelial growth factor (VEGF) during angiogenesis using a rat horizontal OTM model with different force magnitudes. Nickel–titanium coil springs exerting 60 g or 180 g of orthodontic force were applied to the maxillary first molar of 15-week-old male Sprague–Dawley rats; untreated rats served as controls. Tooth movement was evaluated by stereomicroscopy and micro-computed tomography. Senescent cells (p21, p16) and angiogenesis (CD31 and VEGF) were evaluated by multiplex immunofluorescence. Tooth movement was observed under both the 60 g and 180 g conditions. The 60 g group showed increased cellularity, vascular density, and VEGF expression, suggesting an optimal mechanical force. In contrast, the 180 g group reduced cellularity and angiogenesis, consistent with excessive force. Senescent cells were more abundant in the 60 g group, with over 40% expressing VEGF. These findings suggest that force magnitude influences the presence of VEGF+ senescent cells, which may be associated with the angiogenic process in OTM. This work provides insights into the mechanisms underlying optimal force in orthodontic treatment. Full article
(This article belongs to the Special Issue Cellular Senescence in Development, Regeneration, Aging, and Cancer)
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21 pages, 9016 KB  
Article
Mechanistic Study of Hypoxia-Mediated Regulation of Osteoblast Senescence via ATP6V1A-Dependent Modulation of Metabolic Remodeling
by Hefang Xiao, Yi Chen, Xuening Liu, Rongjin Chen, Chenhui Yang, Fei Yang, Changshun Chen, Bin Geng and Yayi Xia
Biology 2025, 14(12), 1801; https://doi.org/10.3390/biology14121801 - 18 Dec 2025
Cited by 1 | Viewed by 812
Abstract
Background: Osteoblast senescence constitutes one of the major mechanisms in bone degeneration and is under tight regulation by metabolism and oxidative stress. While hypoxia has recently emerged as an important microenvironmental factor influencing the function of bone cells, its role in osteoblast senescence [...] Read more.
Background: Osteoblast senescence constitutes one of the major mechanisms in bone degeneration and is under tight regulation by metabolism and oxidative stress. While hypoxia has recently emerged as an important microenvironmental factor influencing the function of bone cells, its role in osteoblast senescence and metabolic regulation has yet to be defined. Methods: The present work entails hypoxia-modulated osteoblast senescence at one level, transcriptomic and metabolomic sequencing, and two levels, in vitro MC3T3-E1 and in vivo AAV-shAtp6v1a mouse models. In transcriptome profiling, hypoxia-responsive genes were identified, whereas non-targeted metabolomics was used to uncover metabolic alterations induced by ATP6V1A knockdown. Oxidative stress and mitochondrial function were assessed by qRT-PCR, Western blotting, SA-β-Gal staining, ROS detection, JC-1 mitochondrial potential, and immunofluorescence. Micro-CT, H&E, Masson, and immunohistochemistry studies were performed to investigate bone structure and protein expression in vivo. Results: Hypoxia markedly mitigated osteoblast senescence, decreasing p53 and p21 expressions and the number of SA-β-Gal-positive cells. It reduced intracellular ROS levels and increased HK2 and LDH expression, decreased ATP, and increased lactate, hinting at a shift toward glycolysis. Transcriptome analysis identified ATP6V1A as one of the major hypoxia-downregulated genes. Knockdown of ATP6V1A reduced ROS levels, inhibited p21 expression, improved mitochondrial function. Metabolomics disclosed remapping pathways in glycolysis, lipid, and amino acid metabolism. Conclusions: This study identifies a “Hypoxia–ATP6V1A–Oxidative Stress–Metabolic Remodeling–Anti-Senescence” axis, demonstrating that hypoxia delays osteoblast senescence by downregulating ATP6V1A, suppressing oxidative stress, and reprogramming metabolism, providing new insights and potential therapeutic targets for bone degenerative diseases. Full article
(This article belongs to the Special Issue Cellular Senescence in Development, Regeneration, Aging, and Cancer)
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