ArticleJournal of cell communication and signaling2020
Et tu, CCN1….
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 1 paper.
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
1 citing paper in PubMed, 3 citations in OpenAlex.
- Role of Matricellular CCN Proteins in Skeletal Muscle: Focus on CCN2/CTGF and Its Regulation by Vasoactive Peptides.International journal of molecular sciences · 2021Review
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
The CCN family of matricellular proteins are recognized bona fide targets for therapeutically targeting so-called chronic inflammatory diseases, including fibrosis and cancers. The majority of the work supporting this contention has been derived from examining CCN2, formerly, and unhelpfully, termed "connective tissue growth factor." Both CCN2, and its related protein, CCN1, formerly termed "cysteine-rich protein 61", are positively regulated by not only TGFbeta, but also by the hippo/YAP/TAZ mechanotransduction pathway that appears to drive these pathologies. Indeed, increasing evidence indicates that CCN1 also contributes to these fibrosis and cancers and, consequently, targeting both CCN2 and CCN1 simultaneously could be of therapeutic value. This commentary focuses on a recent, exciting paper (Ju et al., 2020, Scientific Reports, 10, 3201) suggesting that CCN1 is a target for non-alcoholic steatohepatitis (NASH).
Indexed as
Identifiers
What Socratic 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 Socratic graph.