Evidence map›Paper›PMID 40046513›Full record

ReviewResearch (Washington, D.C.)2025

The Common Hallmarks and Interconnected Pathways of Aging, Circadian Rhythms, and Cancer: Implications for Therapeutic Strategies.

Jie Wang, Fanglin Shao, Qing Xin Yu, Luxia Ye, Dilinaer Wusiman, Ruicheng Wu, Zhouting Tuo, Zhipeng Wang, Dengxiong Li, William C Cho and 2 more

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Research (Washington, D.C.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing 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

42 citing papers in PubMed.

  1. Review
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  11. Mitochondrial function meets oncology: the multifaceted role of TFAM across cancer types.Apoptosis : an international journal on programmed cell death · 2026
    Review
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  19. POSTNFrontiers in immunology · 2026
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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

12 authors.

Jie WangDepartment of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu 610041, China.
Fanglin ShaoDepartment of Rehabilitation, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China.
Qing Xin YuDepartment of Pathology, Ningbo Clinical Pathology Diagnosis Center, Ningbo, Zhejiang 315211, China.
Luxia YeDepartment of Public Research Platform, Taizhou Hospital of Zhejiang Province Affiliated to Wenzhou Medical University, Linhai, China.
Dilinaer WusimanDepartment of Comparative Pathobiology, College of Veterinary Medicine, Purdue University, West Lafayette, IN 47907, USA.
Ruicheng WuDepartment of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu 610041, China.
Zhouting TuoDepartment of Urological Surgery, Daping Hospital, Army Medical Center of PLA, Army Medical University, Chongqing, China.
Zhipeng WangDepartment of Urology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, China.
Dengxiong LiDepartment of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu 610041, China.
William C ChoDepartment of Clinical Oncology, Queen Elizabeth Hospital, Hong Kong SAR, China.
Wuran WeiDepartment of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu 610041, China.
Dechao FengDepartment of Urology, Institute of Urology, West China Hospital, Sichuan University, Chengdu 610041, China.ORCID https://orcid.org/0009-0003-8587-6959

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The intricate relationship between cancer, circadian rhythms, and aging is increasingly recognized as a critical factor in understanding the mechanisms underlying tumorigenesis and cancer progression. Aging is a well-established primary risk factor for cancer, while disruptions in circadian rhythms are intricately associated with the tumorigenesis and progression of various tumors. Moreover, aging itself disrupts circadian rhythms, leading to physiological changes that may accelerate cancer development. Despite these connections, the specific interplay between these processes and their collective impact on cancer remains inadequately explored in the literature. In this review, we systematically explore the physiological mechanisms of circadian rhythms and their influence on cancer development. We discuss how core circadian genes impact tumor risk and prognosis, highlighting the shared hallmarks of cancer and aging such as genomic instability, cellular senescence, and chronic inflammation. Furthermore, we examine the interplay between circadian rhythms and aging, focusing on how this crosstalk contributes to tumorigenesis, tumor proliferation, and apoptosis, as well as the impact on cellular metabolism and genomic stability. By elucidating the common pathways linking aging, circadian rhythms, and cancer, this review provides new insights into the pathophysiology of cancer and identifies potential therapeutic strategies. We propose that targeting the circadian regulation of cancer hallmarks could pave the way for novel treatments, including chronotherapy and antiaging interventions, which may offer important benefits in the clinical management of cancer.

Identifiers

PMID40046513
PMCPMC11880593

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Registered trials

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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 OpenQuestion graph.