Evidence map›Paper›PMID 31546898›Full record

ReviewInternational journal of molecular sciences2019

Regulatory Effects and Interactions of the Wnt and OPG-RANKL-RANK Signaling at the Bone-Cartilage Interface in Osteoarthritis.

Béla Kovács, Enikő Vajda, Előd Ernő Nagy

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed, 4 pooled it
7.3field-weighted citation impact, top 2% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

121 citing papers in PubMed, 4 syntheses or guidelines pooled it, 217 citations in OpenAlex.

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  3. Clinical Data for Parametrization ofFrontiers in bioengineering and biotechnology · 2022
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61 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Béla KovácsDepartment of Biochemistry and Environmental Chemistry, University of Medicine, Pharmacy, Sciences and Technology, Tîrgu Mureș, Romania. bela.kovacs@umfst.ro.ORCID 0000-0003-3881-8636
Enikő VajdaDepartment of Biochemistry and Environmental Chemistry, University of Medicine, Pharmacy, Sciences and Technology, Tîrgu Mureș, Romania. cs_encike@yahoo.com.
Előd Ernő NagyDepartment of Biochemistry and Environmental Chemistry, University of Medicine, Pharmacy, Sciences and Technology, Tîrgu Mureș, Romania. elod.nagy@umfst.ro.
Universitatea de Medicină, Farmacie, Științe și Tehnologie „George Emil Palade” din Târgu Mureș · RO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cartilage and the bordering subchondral bone form a functionally active regulatory interface with a prominent role in osteoarthritis pathways. The Wnt and the OPG-RANKL-RANK signaling systems, as key mediators, interact in subchondral bone remodeling. Osteoarthritic osteoblasts polarize into two distinct phenotypes: a low secretory and an activated, pro-inflammatory and anti-resorptive subclass producing high quantities of IL-6, PGE2, and osteoprotegerin, but low levels of RANKL, thus acting as putative effectors of subchondral bone sclerosis. Wnt agonists, Wnt5a, Wisp-1 initiate excessive bone remodeling, while Wnt3a and 5a simultaneously cause loss of proteoglycans and phenotype shift in chondrocytes, with decreased expression of COL2A, aggrecan, and Sox-9. Sclerostin, a Wnt antagonist possesses a protective effect for the cartilage, while DKK-1 inhibits VEGF, suspending neoangiogenesis in the subchondral bone. Experimental conditions mimicking abnormal mechanical load, the pro-inflammatory milieu, but also a decreased OPG/RANKL ratio in the cartilage, trigger chondrocyte apoptosis and loss of the matrix via degradative matrix metalloproteinases, like MMP-13 or MMP-9. Hypoxia, an important cofactor exerts a dual role, promoting matrix synthesis via HIF-1α, a Wnt silencer, but turning on HIF-2α that enhances VEGF and MMP-13, along with aberrant collagen expression and extracellular matrix deterioration in the presence of pro-inflammatory cytokines.

Indexed as

Wnt Signaling PathwayAnimalsBone and BonesCartilage, ArticularHumansOsteoarthritisOsteoprotegerinRANK LigandReceptor Activator of Nuclear Factor-kappa BWnt ProteinsOsteoprotegerinRANK LigandReceptor Activator of Nuclear Factor-kappa BTNFRSF11A protein, humanTNFRSF11B protein, humanTNFSF11 protein, humanWnt Proteinsbone-cartilage interfaceosteoarthritisWnt signaling

Identifiers

PMID31546898
PMCPMC6769977
OpenAlexW2973915710

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.