Evidence map›Paper›PMID 40356604›Full record

ReviewFrontiers in cell and developmental biology2025

The interplay of cellular senescence and reprogramming shapes the biological landscape of aging and cancer revealing novel therapeutic avenues.

Fuan Ding, Ying Yu, Jiangqi Zhao, Shibo Wei, Yan Zhang, Jung Ho Han, Zhuo Li, Hong-Bo Jiang, Dongryeol Ryu, Minkyoung Cho and 4 more

Abstract readReview
In one paragraph

Review in Frontiers in cell and developmental biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Fuan DingDepartment of Vascular Surgery, The Second Hospital of Jilin University, Changchun, China.
Ying YuDepartment of Surgery, Changchun University of Chinese Medicine, Changchun, China.
Jiangqi ZhaoDepartment of Dermatology, The Second Hospital of Jilin University, Changchun, China.
Shibo WeiDepartment of Biomedical Science and Engineering, Gwangju Institute of Science and Technology, Gwangju, Republic of Korea.
Yan ZhangDepartment of Biomedical Science and Engineering, Gwangju Institute of Science and Technology, Gwangju, Republic of Korea.
Jung Ho HanKorean Medicine Application Center, Korea Institute of Oriental Medicine, Daegu, Republic of Korea.
Zhuo LiDepartment of Nephrology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Hong-Bo JiangDepartment of Dermatology, Qingdao Women and Children's Hospital, Qingdao University, Qingdao, Shandong, China.
Dongryeol RyuDepartment of Biomedical Science and Engineering, Gwangju Institute of Science and Technology, Gwangju, Republic of Korea.
Minkyoung ChoDepartment of Parasitology and Tropical Medicine, and Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju, Republic of Korea.
Sung-Jin BaeDepartment of Molecular Biology and Immunology, Kosin University College of Medicine, Busan, Republic of Korea.
Wonyoung ParkDepartment of Korean Medical Science, School of Korean Medicine, Pusan National University, Yangsan, Gyeongsangnam-do, Republic of Korea.
Ki-Tae HaDepartment of Korean Medical Science, School of Korean Medicine, Pusan National University, Yangsan, Gyeongsangnam-do, Republic of Korea.
Bo GaoDepartment of Vascular Surgery, The Second Hospital of Jilin University, Changchun, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence and cellular reprogramming represent two fundamentally intertwined processes that profoundly influence aging and cancer. This paper explores how the permanent cell-cycle arrest of senescent cells and the identity-resetting capacity of reprogramming jointly shape biological outcomes in later life and tumor development. We synthesize recent findings to show that senescent cells, while halting the proliferation of damaged cells, can paradoxically promote tissue dysfunction and malignancy via their secretory phenotype. Conversely, induced reprogramming of somatic cells-exemplified by Yamanaka factors-resets cellular age and epigenetic marks, offering a potential to rejuvenate aged cells. Key findings highlight shared mechanisms (e.g., DNA damage responses and epigenetic remodeling) and bidirectional crosstalk between these processes: senescence signals can facilitate neighboring cell plasticity, whereas reprogramming attempts can trigger intrinsic senescence programs as a barrier. In aging tissues, transient (partial) reprogramming has been shown to erase senescence markers and restore cell function without inducing tumorigenesis, underlining a novel strategy to combat age-related degeneration. In cancer, we discuss how therapy-induced senescence of tumor cells may induce stem-cell-like traits in some cells and drive relapse, revealing a delicate balance between tumor suppression and tumor promotion. Understanding the interplay between senescence and reprogramming is crucial for developing innovative therapies. By targeting the senescence-reprogramming axis-for instance, via senolytic drugs, SASP inhibitors, or safe reprogramming techniques-there is significant therapeutic potential to ameliorate aging-related diseases and improve cancer treatment. Our findings underscore that carefully modulating cellular senescence and rejuvenation processes could pave the way for novel regenerative and anti-cancer strategies.

Indexed as

agingcancercellular senescencereprogrammingtumor progression

Identifiers

PMID40356604
PMCPMC12066513

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.