ArticleJournal of cell communication and signaling2018
A friend in knee: CCN3 may inhibit osteoarthritis progression.
Article in Journal of cell communication and signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 5 citations in OpenAlex.
- Cellular communication network factor 3 in cartilage development and maintenance.Journal of cell communication and signaling · 2021Review
- CCN3 (NOV) Drives Degradative Changes in Aging Articular Cartilage.International journal of molecular sciences · 2020Article
- WISP1 promotes bovine MDSC differentiation via recruitment of ANXA1 for the regulation of the TGF-β signalling pathway.Molecular and cellular biochemistry · 2020Article
- Higher Serum CCN3 Is Associated with Disease Activity and Inflammatory Markers in Rheumatoid Arthritis.Journal of immunology research · 2020Article
- NOV/CCN3 induces cartilage protection by inhibiting PI3K/AKT/mTOR pathway.Journal of cellular and molecular medicine · 2019Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Osteoarthritis (OA) is a major clinical problem among the ageing population, yet no disease-modifying treatments currently exist. This issue arises, in part, due to the complex processes occurring in the microenvironment of articular cartilage that lead to osteoarthritic changes. Gaining a better understanding of these processes is crucial in developing a viable therapy for OA. A recent report in Journal of Bone Mineral Metabolism by Janune et al. (J Bone Miner Metab 35:582-597, 2016) suggests a novel role for CCN3 in maintaining the differentiated phenotype of articular cartilage. This report suggests that CCN3, a member of the CCN family of matricellular proteins, is important for proteoglycan accumulation, as well as expression of type II collagen, tenascin C, and lubricin in vitro. Furthermore, exogenous CCN3 increased tidemark integrity and lubricin protein expression in a rat model of OA. These results implicate the regulation of CCN3 as a potential therapeutic target in patients with OA.
Indexed as
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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.