ArticleNature communications2018
The senescence-associated secretory phenotype is potentiated by feedforward regulatory mechanisms involving Zscan4 and TAK1.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
What it found
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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.
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Who cites it
95 citing papers in PubMed, 152 citations in OpenAlex.
- The vicious cycle of SASP and inflammaging promotes aging and age-related diseases.Communications biology · 2026Review
- From cell to disease: Regulatory networks and mechanisms of super‑enhancers in aging (Review).Molecular medicine reports · 2026Review
- The role and potential therapeutic intervention of cellular senescence in intervertebral disc degeneration.Genes & diseases · 2026Review
- The natural flavonoid dihydromyricetin targets senescent cells via PRDX2 and alleviates age-related diseases.Nature communications · 2026Article
- Editorial Expression of Concern: The flavonoid procyanidin C1 has senotherapeutic activity and increases lifespan in mice.Nature metabolism · 2026Article
- Targeting age-related LINE-1 activation alleviates cardiac aging.Nature aging · 2026Article
- Integrated Bioinformatic Identification and Experimental Validation Reveal That Aging Exacerbates ARDS Through MAPK14/ADM/MAPK8 Axis.Journal of inflammation research · 2026Article
- Bibliometric Insights into Aging and Immune Function in Prostate Cancer: Focus on Chronic Inflammation.Journal of inflammation research · 2026Review
- Spatial Reorganization of Chromatin Architecture Shapes the Expression Phenotype of Therapy-Induced Senescent Cells.Aging cell · 2026Article
- Natural Products as Anti-Senescence-Associated Secretory Phenotype (SASP) Agents.Current medicinal chemistry · 2026Review
- Balancing senescence and apoptosis: therapeutic insights into aging and cancer.Molecular and cellular biochemistry · 2025Review
- Dual inhibition of IRAK1/TAK1 signaling in astrocytes reduces accelerated mortality in human APOE4 knock-in APPswe/PSEN1dE9/P301S-Tau triple transgenic mouse model.Journal of neuroinflammation · 2025Article
- Tissue specificity and chromosomal alterations shape divergent immune programs in HRD tumors.bioRxiv : the preprint server for biology · 2025Article
- KDM4 Orchestrates Epigenomic Remodeling of Senescent Cells and Potentiates the Senescence-Associated Secretory Phenotype.Aging cell · 2025Article
- Pyrroloquinoline Quinone Is an Effective Senomorphic Agent to Target the Pro-Inflammatory Phenotype of Senescent Cells.Aging cell · 2025Article
- 3D models to study therapy-induced senescence: where do we stand now?Cytotechnology · 2025Review
- ZSCAN4 functions as a safeguard to maintain centromere integrity during oocyte meiosis.Genome biology · 2025Article
- Macrophage-targeting Antisenescence nanomedicine enables in-Situ NO induction for Gaseous and antioxidative atherosclerosis intervention.Bioactive materials · 2025Article
- New Insights into the Role of Cellular Senescence and Its Therapeutic Implications in Ocular Diseases.Bioengineering (Basel, Switzerland) · 2025Review
- Targeting Senescence with Apigenin Improves Chemotherapeutic Efficacy and Ameliorates Age-Related Conditions in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
35 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 3 countries.
Funding
Abstract
The senescence-associated secretory phenotype (SASP) can be provoked by side effects of therapeutic agents, fueling advanced complications including cancer resistance. However, the intracellular signal network supporting initiation and development of the SASP driven by treatment-induced damage remains unclear. Here we report that the transcription factor Zscan4 is elevated for expression by an ATM-TRAF6-TAK1 axis during the acute DNA damage response and enables a long term SASP in human stromal cells. Further, TAK1 activates p38 and PI3K/Akt/mTOR to support the persistent SASP signaling. As TAK1 is implicated in dual feedforward mechanisms to orchestrate the SASP development, pharmacologically targeting TAK1 deprives cancer cells of resistance acquired from treatment-damaged stromal cells in vitro and substantially promotes tumour regression in vivo. Together, our study reveals a novel network that links functionally critical molecules associated with the SASP development in therapeutic settings, thus opening new avenues to improve clinical outcomes and advance precision medicine.
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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.