ArticleJournal of cell communication and signaling2011
CCN2: a bona fide target for anti-fibrotic drug intervention.
Article in Journal of cell communication and signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 10 citations in OpenAlex.
- New Functions of Classical Compounds against Orofacial Inflammatory Lesions.Medicines (Basel, Switzerland) · 2018Review
- Matricellular proteins in drug delivery: Therapeutic targets, active agents, and therapeutic localization.Advanced drug delivery reviews · 2016Review
- Autophagy fosters myofibroblast differentiation through MTORC2 activation and downstream upregulation of CTGF.Autophagy · 2014Article
- Cutaneous wound healing: recruiting developmental pathways for regeneration.Cellular and molecular life sciences : CMLS · 2013Review
- Eureka! Ets a target for fibrosis!Journal of cell communication and signaling · 2011Article
- CCN2/decorin interactions: a novel approach to combating fibrosis?Journal of cell communication and signaling · 2011Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
CCN2 (formerly known as connective tissue growth factor) was identified by several different laboratories approximately 20 years ago. Almost since its identification as a factor induced in normal fibroblasts by transforming growth factor β and overexpressed in fibrotic disease, CCN2 has been hypothesized to be not only a marker but also a central mediator of fibrosis in vivo. Finally, in vivo data are emerging to validate this key hypothesis. For example, a neutralizing anti-CCN2 antibody was found to attenuate fibrogenesis in three separate animal models (Wang et al. in Fibrogenesis Tissue Repair 4:1-4, 2011). This commentary addresses recent data indicating that CCN2 appears to represent a key central mediator of fibrosis and a good target for anti-fibrotic drug intervention.
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.