ArticleJournal of cell communication and signaling2017
CCN2 induces cellular senescence in fibroblasts.
Article in Journal of cell communication and signaling, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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.
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.
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Who cites it
44 citing papers in PubMed, 69 citations in OpenAlex.
- The vicious cycle of SASP and inflammaging promotes aging and age-related diseases.Communications biology · 2026Review
- SenSet defines cell-type specific senescence signatures in the aged human lung.The EMBO journal · 2026Article
- The matricellular protein CCN5 (WISP2) inhibits cellular senescence in cardiac myoblasts and fibroblasts.Scientific reports · 2026Article
- Review
- Defective RNA processing and ELOA-mediated transcriptional elongation in reversible cellular senescence suggest aging by transcription.Molecular cell · 2025Article
- Plasminogen activator inhibitor 1 promotes aortic aging-like pathophysiology in humans and mice.The Journal of clinical investigation · 2025Article
- Heterogeneity of Cellular Senescence, Senotyping, and Targeting by Senolytics and Senomorphics in Lung Diseases.International journal of molecular sciences · 2025Review
- Cells of all trades - on the importance of spatial positioning of senescent cells in development, healing and aging.FEBS letters · 2025Review
- CCN2 Activates Cellular Senescence Leading to Kidney Fibrosis in Folic Acid-Induced Experimental Nephropathy.International journal of molecular sciences · 2025Article
- The contribution of amphibian macrophage subsets to scarless regeneration of skin wounds.Frontiers in immunology · 2025Article
- Involvement of Matricellular Proteins in Cellular Senescence: Potential Therapeutic Targets for Age-Related Diseases.International journal of molecular sciences · 2024Review
- The cholesterol biosynthesis enzyme FAXDC2 couples Wnt/β-catenin to RTK/MAPK signaling.The Journal of clinical investigation · 2024Article
- Clearance of senescent cells enhances skin wound healing in type 2 diabetic mice.Theranostics · 2024Article
- Embryonic stem cell-derived extracellular vesicles rejuvenate senescent cells and antagonize aging in mice.Bioactive materials · 2023Article
- The aged extracellular matrix and the profibrotic role of senescence-associated secretory phenotype.American journal of physiology. Cell physiology · 2023Review
- Protein-Bound Uremic Toxins in Senescence and Kidney Fibrosis.Biomedicines · 2023Review
- Article
- CCN proteins: opportunities for clinical studies-a personal perspective.Journal of cell communication and signaling · 2023Review
- Cellular and Molecular Mechanisms in Idiopathic Pulmonary Fibrosis.Advances in respiratory medicine · 2023Review
- Multifaceted roles of mitochondria in wound healing and chronic wound pathogenesis.Frontiers in cell and developmental biology · 2023Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The expression of Ccn2 (CTGF) has been linked to fibrosis in many tissues and pathologies, although its activities in fibroblastic cells and precise mechanism of action in fibrogenesis are still controversial. Here, we showed that CCN2 can induce cellular senescence in fibroblasts both in vitro and in vivo, whereupon senescent cells express an anti-fibrotic "senescence-associated secretory phenotype" (SASP) that includes upregulation of matrix metalloproteinases and downregulation of collagen. Mechanistically, CCN2 induces fibroblast senescence through integrin α
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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.