ArticleJournal of cell communication and signaling2020
Slow train coming: an anti-CCN2 strategy reverses a model of chronic overuse muscle fibrosis.
Article in Journal of cell communication and signaling, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 7 citations in OpenAlex.
- A pH-sensitive peptide amphiphilic-based drug delivery system inhibits hepatocellular carcinoma growth by suppressing hepatic stellate cell activation.Materials today. Bio · 2025Article
- CCN2/CTGF expression does not correlate with fibrosis in myeloproliferative neoplasms, consistent with noncanonical TGF-β signaling driving myelofibrosis.Virchows Archiv : an international journal of pathology · 2024Article
- Let's Focus on the Fibrosis in Dupuytren Disease: Cell Communication Network Factor 2 as a Novel Target.Journal of hand surgery global online · 2023Review
- CCN proteins: opportunities for clinical studies-a personal perspective.Journal of cell communication and signaling · 2023Review
- The impaired healing hypothesis: a mechanism by which psychosocial stress and personal characteristics increase MSD risk?Ergonomics · 2022Article
- Selective deletion of connective tissue growth factor attenuates experimentally-induced pulmonary fibrosis and pulmonary arterial hypertension.The international journal of biochemistry & cell biology · 2021Article
- Connective Tissue Growth Factor: From Molecular Understandings to Drug Discovery.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
One of the first targets proposed as an anti-fibrotic therapy was CCN2. Proof of its involvement in fibrosis was initially difficult, due to the lack of appropriate reagents and general understanding of the molecular mechanisms responsible for persistent fibrosis. As these issues have been progressively resolved over the last twenty-five years, it has become clear that CCN2 is a bone fide target for anti-fibrotic intervention. An anti-CCN2 antibody (FG-3019) is in Phase III clinical trials for idiopathic pulmonary fibrosis and pancreatic cancer, and in Phase II for Duschenne's muscular dystrophy. An exciting paper recently published by Mary Barbe and the Popoff group has shown that FG-3019 reduces established muscle fibrosis (Barbe et al., FASEB J 34:6554-6569, 2020). Intriguingly, FG-3019 blocked the decreased expression of the anti-fibrotic protein CCN3, caused by the injury model. These important data support the notion that targeting CCN2 in the fibrotic microenvironment may reverse established fibrosis, making it the first agent currently in development to do so.
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.