Special Issues
Table of Content

Cellular Senescence in Health and Disease

Submission Deadline: 15 March 2026 View: 1107 Submit to Special Issue

Guest Editors

Assoc. Prof. Hongli Wu

Email: Hongli.Wu@unthsc.edu

Affiliation: Pharmaceutical Sciences, College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX 76107, USA

North Texas Eye Research Institution, Fort Worth, TX 76107, USA

Homepage:

Research Interests: cellular senescence, oxidative stress, chronic inflammation, and a premature mouse model, senotherapeutic

图片3.png


Dr. Ying Qin

Email: yingqin@my.unthsc.edu

Affiliation: Pharmaceutical Sciences, College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX 76107, USA 

College of Biomedical and Translational Sciences, University of North Texas Health Science Center, Fort Worth, Tx 76107, USA

North Texas Eye Research Institution, Fort Worth, TX 76107, USA

Homepage:

Research Interests: cellular senescence, chronic inflammation, oxidative stress, premature mouse model, senotherapeutics, neurodegeneration

图片4.jpg


Dr. Haoxin Liu

Email: haoxin.liu@nyulangone.org

Affiliation: Department of Pharmacy, NYU Langone Hospital-Brooklyn, Brooklyn, NY 11220, USA

Homepage: www.linkedin.com/in/haoxin-liu-972107218

Research Interests: Cellular senescence, oxidative stress, nephrology in mouse model, clinical infectious diseases, chronic disease management

图片5.jpg


Summary

Cellular senescence, a state of stable cell cycle arrest accompanied by profound changes in cell function, has emerged as a pivotal biological process influencing both health and disease. While initially recognized as a natural tumor-suppressive mechanism, senescence now is understood to play multifaceted roles in aging, tissue homeostasis, and chronic pathological conditions. The accumulation of senescent cells contributes to tissue dysfunction and the progression of diseases such as cancer, fibrosis, metabolic syndromes, and neurodegeneration. Recent advances in molecular biology and therapeutics have paved the way for innovative strategies targeting senescent cells—termed senotherapeutics, offering promising avenues for intervention.

This special issue aims to integrate research efforts that deepen our understanding of the molecular and cellular underpinnings of cellular senescence and its dual roles in physiology and pathology. The issue will cover the following key subtopics:
1. Molecular Mechanisms of Cellular Senescence: Exploring the signaling pathways, DNA damage responses, epigenetic modifications, and metabolic shifts that initiate and maintain the senescent state. Studies elucidating the regulation of the senescence-associated secretory phenotype (SASP) will also be highlighted.
2. Senescence in Tissue Homeostasis and Aging: Investigations into how senescence contributes to normal development, wound healing, and age-related functional decline. The balance between beneficial and detrimental effects of senescent cells in various tissues will be examined.
3. Senescence in Disease Pathogenesis: Reviews and original research detailing the role of senescent cells in cancer progression and suppression, fibrotic diseases, metabolic dysfunction, and neurodegenerative disorders. This section emphasizes the interplay between senescence and the immune system in disease contexts.
4. Senotherapeutics and Therapeutic Strategies: This section emphasizes the molecular and cellular mechanisms of senolytic and senomorphic agents targeting senescent cells. Studies on how these therapies modulate key signaling pathways, SASP, and tissue microenvironments are welcome. Both preclinical mechanistic work and early clinical data elucidating therapeutic efficacy and specificity will be featured.
5. Biomarkers and Model Systems for Senescence: We invite research on molecular and cellular biomarkers that accurately identify senescence in vivo, including those from transcriptomics, proteomics, and epigenetics. Also encouraged are advanced in vitro and in vivo models that enable detailed mechanistic studies and evaluation of senescence-targeted therapies, aligned with BIOCELL's cellular and molecular focus.

In summary, this special issue will provide a comprehensive and multidisciplinary perspective on cellular senescence, bridging fundamental molecular insights with translational research and therapeutic innovation. It aligns with BIOCELL's mission to unravel life processes and disease mechanisms at the cellular and molecular levels, fostering novel approaches to improve human health.


Keywords

cellular senescence, SASP, senotherapeutics, aging, cancer, biomarkers, DNA damage response

Published Papers


  • Open Access

    REVIEW

    The Yin–Yang of Stress and Senescence: Integrated Stress Response and SASP Crosstalk in Stem Cell Fate, Regeneration, and Disease

    Douglas M. Ruden
    BIOCELL, DOI:10.32604/biocell.2025.072273
    (This article belongs to the Special Issue: Cellular Senescence in Health and Disease)
    Abstract Stem cell fate decisions are increasingly understood through the dynamic interplay of two fundamental stress-adaptive programs: the integrated stress response (ISR) and the senescence-associated secretory phenotype (SASP). These pathways act as a Yin–Yang system, balancing beneficial and detrimental outcomes across development, tissue homeostasis, and disease. On the yin (protective) side, transient ISR activation and acute SASP signaling foster adaptation, embryonic patterning, wound healing, and regeneration. On the yang (maladaptive) side, chronic ISR signaling and unresolved SASP output drive stem cell exhaustion, fibrosis, inflammation, and tumorigenesis. This duality highlights their roles as both guardians and disruptors More >

    Graphic Abstract

    The Yin–Yang of Stress and Senescence: Integrated Stress Response and SASP Crosstalk in Stem Cell Fate, Regeneration, and Disease

  • Open Access

    ARTICLE

    Death Ligand Signaling Involving the COX/PKC/MLKL Axis Mediates Erythrocyte Death by HDAC/DNMT Inhibitor, Parthenolide, through ROS Generation and Calcium Mobilization

    Sara Y. Aldeghaither, Jawaher Alsughayyir, Sabiha Fatima, Mohammad A. Alfhili
    BIOCELL, Vol.49, No.11, pp. 2167-2180, 2025, DOI:10.32604/biocell.2025.071827
    (This article belongs to the Special Issue: Cellular Senescence in Health and Disease)
    Abstract Objectives: Targeting epigenetic modifications in anticancer therapy is a promising approach to overcoming cancer cell chemoresistance. The histone deacetylase/DNA methyltransferase inhibitor, parthenolide (PTL), has antitumor activity, but contrasting findings exist on its effect in normal cells. This study aims to examine the non-genomic toxic mechanisms of PTL in human erythrocytes. Methods: Cell death as stimulated by 20–200 μM of PTL for 24 h at 37°C was assessed using fluorescence-assorted cell sorting and spectrophotometric assays. Canonical markers of cell death, including membrane scrambling, oxidative stress, and Ca2+ mobilization, were captured by annexin V-fluorescein isothiocyanate, 2,7-dichlorodihydrofluorescein diacetate, and… More >

Share Link