ReviewBoneKEy reports2014
Wnts' fashion statement: from body stature to dysplasia.
Review in BoneKEy reports, 2014. 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, 8 citations in OpenAlex.
- Increased Expression of Sox9 during Balance of BMSCs/Chondrocyte Bricks in Platelet-Rich Plasma Promotes Construction of a Stable 3-D Chondrogenesis Microenvironment for BMSCs.Stem cells international · 2020Article
- IL-1β Enhances Wnt Signal by Inhibiting DKK1.Inflammation · 2018Article
- The multi-faceted role of retinoid X receptor in bone remodeling.Cellular and molecular life sciences : CMLS · 2017Review
- Inactivation of Fam20B in Joint Cartilage Leads to Chondrosarcoma and Postnatal Ossification Defects.Scientific reports · 2016Article
- Establishment of a porcine pancreatic stem cell line using T-REx(™) system-inducible Wnt3a expression.Cell proliferation · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Bone is constantly being made and remodeled to maintain bone volume and calcium homeostasis. Even small changes in the dosage, location and duration of int/Wingless (Wnt) signaling affect skeletal development and homeostasis. Wnt/β-catenin signaling controls cell fate determination, proliferation and survival by affecting a balance between bone-forming osteoblast and bone-resorbing osteoclast cell differentiation. During early skeletal development, Wnt/β-catenin signaling is required in directing mesenchymal progenitor cells toward the osteoblast lineage. Later, Wnt/β-catenin in chondrocytes of the growth plate promotes chondrocyte survival, hypertrophic differentiation and endochondral ossification. Gain- or loss-of-function mutations in the Wnt signaling components are causally linked to high or low bone mass in mice and humans. Inactivation of Wnt/β-catenin signaling leads to imbalance between bone formation and resorption because of accelerated osteoclastogenesis due to decline in the levels of osteoprotegerin (OPG) secreted by osteoblasts or directly via Frizzled 8 (Fzd8). In this review, we provide a landscape of the Wnt pathway components in influencing progenitor cell differentiation toward osteoblasts or osteoclasts under physiological conditions as well as pathological disorders resulting in various skeletal dysplasia syndromes.
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.