Cellular Senescence and Transformation: Unraveling the Biological Links Between Aging and Cancer

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 10 May 2026 | Viewed by 720

Special Issue Editors

College of Life and Health Sciences, Northeastern University, Shenyang 110167, China
Interests: embryo development; genome editing; epigenetics; cancer; stem cells; somatic cell nuclear transfer; oxidative stress; pig; natural products; phase separation
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Health Sciences Institute, China Medical University, Shenyang 110122, China
Interests: aging; neurodegenerative diseases; α-synuclein aggregation; phase seperation; non-membraneless organelles; genome editing; animal model

E-Mail Website
Guest Editor
College of Life and Health Sciences, Northeastern University, Shenyang 110167, China
Interests: tyrosine phosphatase; autoimmune diseases; protein interactions; TCR signaling pathway; T cell development; T cell activation; T cell differentiation; inflammation; membrane transport; nuclear transport; cancer

Special Issue Information

Dear Colleagues,

Aging and cancer, two complex biological processes, share an intimate and paradoxical relationship. While advanced age is the single greatest risk factor for most cancers, the underlying cellular and molecular mechanisms driving this connection remain a central question in biomedical research. This interplay involves a delicate balance: hallmarks of aging, such as genomic instability, epigenetic alterations, and cellular senescence, can create a permissive environment for oncogenesis. Conversely, mechanisms that suppress cancer often overlap with those that promote aging.

In this Special Issue, original research articles, comprehensive reviews, communications, and systematic reviews are welcome. Research areas may include but are not limited to the following:

  • Cellular senescence;
  • Aging and cancer;
  • Cellular reprogramming;
  • Gene editing;
  • Epigenetics;
  • Cancer therapy;
  • Oxidative stress;
  • DNA damage response;
  • Metabolism;
  • Immune surveillance;
  • Microenvironment;
  • Protein aggregation.

We look forward to receiving your contributions.

Dr. Yongye Huang
Dr. Lin Yuan
Dr. Yang Yu
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 250 words) can be sent to the Editorial Office for assessment.

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. Cells 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

  • aging
  • cancer
  • stem cells
  • gene editing
  • oncogene
  • apoptosis
  • targeted therapy
  • epigenetics

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

20 pages, 11395 KB  
Article
TIA1 Mutant Mouse Model Exhibits Motor Deficits and Neurodegenerative Characteristics of Amyotrophic Lateral Sclerosis
by Li-Hong Mao, Yu-Ning Song, Jing-Qi Zhang, Yun-Ting Shao, Zhang-Li Wang, Na Yang, Wen-Xuan Zhang, Ying-Rui Zhang, Xiao-Yan Gao, Jia-Yi Li and Lin Yuan
Cells 2026, 15(5), 420; https://doi.org/10.3390/cells15050420 - 27 Feb 2026
Viewed by 438
Abstract
Background: Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease that primarily affects the motor neurons. T cell intracellular antigen 1 (TIA1) is a risk gene for ALS pathogenesis. To elucidate TIA1-mediated disease mechanisms, a mouse model recapitulating clinical and pathological features of [...] Read more.
Background: Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease that primarily affects the motor neurons. T cell intracellular antigen 1 (TIA1) is a risk gene for ALS pathogenesis. To elucidate TIA1-mediated disease mechanisms, a mouse model recapitulating clinical and pathological features of ALS is needed. TIA1 mutations are rare in human ALS, and mutations are heterozygous, while this study uses a homozygous TIA1 mutant mouse model to amplify pathogenic effects for experimental tractability. Methods: To explore the mechanisms by which mutant TIA1 causes ALS neurodegeneration, we generated a TIA1 mutant mouse by introducing ALS-causing mutations into the endogenous animal via cytosine base editors. Next, behavioral experiments (open-field and rotarod tests) assessed motor function and analyzed pathologies using morphological assessments. Results: Our TIA1Δ mouse model phenocopies select pivotal features of ALS, including TAR DNA-binding protein 43 (TDP-43) accumulation, motor neuron loss, neuroinflammation in the lumbar spinal cord, and muscle atrophy. Notably, this homozygous mutation design with reduced TIA1 expression differs from human heterozygous TIA1 mutations. Conclusions: This work provides a foundation for understanding the TIA1-ALS relationship and for developing strategies to treat this intractable neurodegenerative disorder. Caution is warranted extrapolating findings to human ALS pathogenesis due to model design differences. Full article
Show Figures

Graphical abstract

Back to TopTop