ReviewJournal of biochemistry2025
Cellular senescence: mechanisms and relevance to cancer and aging.
Review in Journal of biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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.
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.
Who cites it
30 citing papers in PubMed.
- Article
- Review
- Exploring Stem Cell Based Senotherapeutic Strategies for Targeting Cellular Senescence in Brain Aging.Stem cell reviews and reports · 2026Review
- Anti-aging effects of glycyrrhizin via maintaining Klotho levels.Journal of clinical biochemistry and nutrition · 2026Article
- Review
- Fate Bifurcation of Cellular Senescence: Dynamic Regulation from Tumor Suppression to Recurrence Risk.Cells · 2026Review
- Next-generation therapies for osteoarthritis: the evolving role of cell therapy products.Experimental & molecular medicine · 2026Review
- Diverse Forms of Autophagy and Their Roles in Liver Disease and Aging: A Comprehensive Review.Proteomes · 2026Review
- cGAS-STING Signaling as a Molecular Bridge Between Inflammation, Ovarian Ageing, and Reproductive Failure.International journal of molecular sciences · 2026Review
- A machine learning-driven framework integrating cell death and senescence signatures for multi-target drug design and immunotherapy optimization in ovarian cancer.NPJ precision oncology · 2026Article
- Upregulation of CSN8 induces a unique senescence-like state with robust tumor-promoting properties in epithelial ovarian cancer cells under hypoxia.Journal of translational medicine · 2026Article
- Exercise, Cellular Senescence, and Cancer: Novel Perspectives on Functional Aging Through Block Strength Training in Older Adults-A Narrative Review.Biomedicines · 2026Review
- Neuroendocrine-associated epigenetic factors in cellular senescence: mechanisms and therapeutic implications.Biogerontology · 2026Review
- Evolutionary perspectives on endometrial cancer: antagonistic pleiotropy.Molecular & cellular oncology · 2026Review
- Filamin a binds deleted in liver cancer 1 (DLC1) to promote its tumor suppressor activity and inhibit the SRF coactivator MRTF-A.Neoplasia (New York, N.Y.) · 2026Article
- Editorial: Empowering cancer care through immunonutrition.Frontiers in nutrition · 2026Article
- Immune monitoring for relapse of acute myeloid leukemia after allogeneic stem cell transplantation in clinical laboratories.Frontiers in immunology · 2026Review
- PI3K/mTOR inhibition attenuates cigarette smoke-induced senescence and SASP in oral fibroblasts: implications for tumor microenvironment remodeling.Frontiers in cell and developmental biology · 2026Article
- Design and Synthesis of New Coumarin Hybrids Active Against Drug-Sensitive and Drug-Resistant Neuroblastoma Cells.Antioxidants (Basel, Switzerland) · 2025Article
- Molecular Mechanisms Driving Metastatic Progression Within the Aged Tumor Microenvironment.International journal of molecular sciences · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Cellular senescence is an irreversible cell cycle arrest induced by stresses such as telomere shortening and oncogene activation. It acts as a tumor suppressor mechanism that prevents the proliferation of potentially tumorigenic cells. Paradoxically, senescent stromal cells that arise in the tumor microenvironment have been shown to promote tumor progression. In addition, senescent cells that accumulate in vivo over time are thought to contribute to aging and age-related diseases. These deleterious effects of senescent cells involve the secretion of bioactive molecules such as inflammatory cytokines and chemokines, a phenomenon known as the senescence-associated secretory phenotype. While the role of cellular senescence in vivo is becoming increasingly clear, the intracellular signaling pathways that induce the expression of senescent phenotypes are not fully understood. In this review, we outline senescence-associated signaling pathways and their relevance to cancer and aging.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.