ArticleNature cell biology2010
The matricellular protein CCN1 induces fibroblast senescence and restricts fibrosis in cutaneous wound healing.
Article in Nature cell biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 548 papers, 3 of them syntheses that pooled 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.
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
548 citing papers in PubMed, 3 syntheses or guidelines pooled it, 945 citations in OpenAlex.
- A Systematic Review of the Role of Senescent Cells in Uterine Leiomyomas: Deciphering Molecular Pathways and Exploring Therapeutic Prospects.Reproductive sciences (Thousand Oaks, Calif.) · 2026Pooled it
- Proteomic Analysis of the Senescence-Associated Secretory Phenotype: GDF-15, IGFBP-2, and Cystatin-C Are Associated With Multiple Aging Traits.The journals of gerontology. Series A, Biological sciences and medical sciences · 2024Pooled it
- Identification of Hub Genes in Idiopathic Pulmonary Fibrosis and Their Association with Lung Cancer by Bioinformatics Analysis.Advances in respiratory medicine · 2023Pooled it
- LncRNA Gm44981 modulates EZH2-H3K27me3-p21 axis to suppress mesangial cell senescence and kidney aging.Renal failure · 2026Article
- Cellular senescence: six decades of discovery and reinvention.The EMBO journal · 2026Review
- Cellular communication network factor 1 (CCN1) associates with all-cause mortality in patients with dilated cardiomyopathy.International journal of cardiology. Heart & vasculature · 2026Article
- Critical role of cellular communication network factor 1 in early osteogenesis of mesenchymal stem cells primed by low-intensity pulsed ultrasound and bone morphogenetic protein 2.Journal of cell communication and signaling · 2026Article
- Preliminary outcomes and transcriptomic analysis of xenogeneic human-derived acellular dermal matrix patches for complex ureteral stricture reconstruction in a porcine model.Translational andrology and urology · 2026Article
- NAMPT activation uncovers a senescence-specific vulnerability and promotes healthy aging in combination with NAM.bioRxiv : the preprint server for biology · 2026Article
- The Matricellular Protein CCN1 Induces Corneal Stromal Cells Senescence and Inflammation to Trigger Extracellular Matrix Remodeling in Keratoconus.Investigative ophthalmology & visual science · 2026Article
- The aging extracellular matrix as a missing link in senescent cell accumulation and persistence.Nature aging · 2026Article
- Royal jelly suppresses senescence-associated secretory phenotype in senescent human epidermal keratinocytes.Molecular biology reports · 2026Article
- Review
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- Fibroblasts as regulators of lung immunity, repair and fibrosis.Nature reviews. Immunology · 2026Review
- Extracellular ATP drives tryptophan metabolism and aryl hydrocarbon receptor activation to promote cellular senescence.The Journal of biological chemistry · 2026Article
- Multi-biomarker approach for predicting cardiac magnetic resonance parameters at 30 days after ST-segment elevation myocardial infarction.International journal of cardiology. Heart & vasculature · 2026Article
- Cellular senescence in skeletal muscle regeneration.Cell regeneration (London, England) · 2026Review
- CD8Science China. Life sciences · 2026Review
488 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cellular senescence is a recognized mechanism of tumour suppression; however, its contribution to other pathologies is not well understood. We show that the matricellular protein CCN1 (also known as CYR61; cysteine-rich protein 61), which is dynamically expressed at sites of wound repair, can induce fibroblast senescence by binding to integrin alpha(6)beta(1) and the heparan sulphate proteoglycans (receptors involved in cell adhesion). CCN1 induces DNA damage response pathways and activates p53 and the RAC1-NOX1 complex, which generates reactive oxygen species (ROS). This results in the ROS-dependent activation of the p16(INK4a)/pRb pathway, leading to senescence and concomitant expression of antifibrotic genes. Senescent fibroblasts accumulate in granulation tissues of healing cutaneous wounds and express antifibrotic genes in wild-type mice. These processes are lost in knockin mice that express a senescence-defective Ccn1 mutant, resulting in exacerbated fibrosis. Topical application of CCN1 protein to wounds reverses these defects. Thus, fibroblast senescence is a CCN1-dependent wound healing response in cutaneous injury that functions to curb fibrosis during tissue repair.
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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.