ReviewAgeing research reviews2015
DAMPs, ageing, and cancer: The 'DAMP Hypothesis'.
Review in Ageing research reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 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
84 citing papers in PubMed.
- Cost-Effectiveness Analysis of First-Line FOLFIRI Combined With Cetuximab or Bevacizumab in Patients With RAS Wild-Type Left-Sided Metastatic Colorectal Cancer.Cancer control : journal of the Moffitt Cancer CenterTrial
- Temporal Vulnerability of the Blood-Brain Interface in Stroke: Molecular Mechanisms of Circadian Dynamics, Inflammation, and Aging.International journal of molecular sciences · 2026Review
- Mitochondria as Inducers of Neutrophil Extracellular Traps.Inflammation · 2026Review
- Towards a personalized perspective on gliomas: an epigenetic-immuno-inflammatory aging framework.Frontiers in immunology · 2026Review
- Heat shock proteins in farmed aquatic animals: advancing animal health and welfare management through building resilience.Frontiers in immunology · 2026Review
- Neutrophil Senescence Induced by Tumor-Derived HMGB1 Promotes Hepatocellular Carcinoma Progression through Neutrophil Extracellular Trap-Mediated Suppression of CD8Cancer communications (London, England) · 2026Article
- Modulation of Toll-like Receptors with Natural Compounds: A Therapeutic Avenue Against Inflammaging?International journal of molecular sciences · 2025Review
- Adipose immune microenvironment: catalyst of age-related adipose tissue dysfunction.Immunity & ageing : I & A · 2025Review
- Salidroside alleviates cardiomyocyte senescence by activating the AMPK-mediated signaling pathway.Journal of molecular histology · 2025Article
- Pattern recognition receptors: function, regulation and therapeutic potential.Signal transduction and targeted therapy · 2025Review
- Chondrocyte lysates activate NLRP3 inflammasome-induced pyroptosis in synovial fibroblasts to exacerbate knee synovitis by downregulating caveolin-1.Arthritis research & therapy · 2025Article
- Critical roles of chronic BCR signaling in the differentiation of anergic B cells into age-associated B cells in aging and autoimmunity.Science advances · 2025Article
- Dengue virus infection: how platelet-leukocyte crosstalk shapes thrombotic events and inflammation.Molecular biology reports · 2025Review
- Collagen I-Derived Extracellular Matrix Motifs Alter Fibroblast Regenerative Response.Cells, tissues, organs · 2025Article
- S100A proteins show a spatial distribution of inflammation associated with the glioblastoma microenvironment architecture.Theranostics · 2025Article
- Immune aging and infectious diseases.Chinese medical journal · 2024Review
- Different clinical presentations of Achilles tendinopathy: a cross-sectional study.Rheumatology international · 2024Article
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- The war between the immune system and the tumor - using immune biomarkers as tracers.Biomarker research · 2024Review
24 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Ageing is a complex and multifactorial process characterized by the accumulation of many forms of damage at the molecular, cellular, and tissue level with advancing age. Ageing increases the risk of the onset of chronic inflammation-associated diseases such as cancer, diabetes, stroke, and neurodegenerative disease. In particular, ageing and cancer share some common origins and hallmarks such as genomic instability, epigenetic alteration, aberrant telomeres, inflammation and immune injury, reprogrammed metabolism, and degradation system impairment (including within the ubiquitin-proteasome system and the autophagic machinery). Recent advances indicate that damage-associated molecular pattern molecules (DAMPs) such as high mobility group box 1, histones, S100, and heat shock proteins play location-dependent roles inside and outside the cell. These provide interaction platforms at molecular levels linked to common hallmarks of ageing and cancer. They can act as inducers, sensors, and mediators of stress through individual plasma membrane receptors, intracellular recognition receptors (e.g., advanced glycosylation end product-specific receptors, AIM2-like receptors, RIG-I-like receptors, and NOD1-like receptors, and toll-like receptors), or following endocytic uptake. Thus, the DAMP Hypothesis is novel and complements other theories that explain the features of ageing. DAMPs represent ideal biomarkers of ageing and provide an attractive target for interventions in ageing and age-associated diseases.
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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.