ArticleActualizaciones en osteologia2011
CONNEXIN 43 AND BONE: NOT JUST A GAP JUNCTION PROTEIN.
Article in Actualizaciones en osteologia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed, 16 citations in OpenAlex.
- Investigating mechanical and inflammatory pathological mechanisms in osteoarthritis using MSC-derived osteocyte-like cells in 3D.Frontiers in endocrinology · 2024Article
- Connexin 43 in the function and homeostasis of osteocytes: a narrative review.Annals of joint · 2024Review
- The Mechanotransduction Signaling Pathways in the Regulation of Osteogenesis.International journal of molecular sciences · 2023Review
- Osteocytes Exposed to Titanium Particles Inhibit Osteoblastic Cell Differentiation via Connexin 43.International journal of molecular sciences · 2023Article
- The altered osteocytic expression of connexin 43 and sclerostin in human cadaveric donors with alcoholic liver cirrhosis: Potential treatment targets.Journal of anatomy · 2022Article
- Bone fracture healing: perspectives according to molecular basis.Journal of bone and mineral metabolism · 2021Review
- A 3D, Dynamically Loaded Hydrogel Model of the Osteochondral Unit to Study Osteocyte Mechanobiology.Advanced healthcare materials · 2020Article
- IDG-SW3 Osteocyte Differentiation and Bone Extracellular Matrix Deposition Are Enhanced in a 3D Matrix Metalloproteinase-Sensitive Hydrogel.ACS applied bio materials · 2020Article
- Ginkgolide B Inhibits JAM-A, Cx43, and VE-Cadherin Expression and Reduces Monocyte Transmigration in Oxidized LDL-Stimulated Human Umbilical Vein Endothelial Cells.Oxidative medicine and cellular longevity · 2015Article
- Evidence for the role of connexin 43-mediated intercellular communication in the process of intracortical bone resorption via osteocytic osteolysis.BMC musculoskeletal disorders · 2014Article
- Article
- Determining how defects in connexin43 cause skeletal disease.Genesis (New York, N.Y. : 2000) · 2013Review
- Connexin 43 plays a role in proliferation and migration of pulmonary arterial fibroblasts in response to hypoxia.Pulmonary circulationArticle
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
Abstract
Connexins are essential for the communication of cells among themselves and with their environment. Connexin hexamers assemble at the plasma membrane to form hemichannels that allow the exchange of cellular contents with the extracellular milieu. In addition, hemichannels expressed in neighboring cells align to form gap junction channels that mediate the exchange of contents among cells. Connexin 43 (Cx43) is the most abundant connexin expressed in bone cells and its deletion in all tissues leads to osteoblast dysfunction, as evidenced by reduced expression of osteoblast markers and delayed ossification. Moreover, Cx43 is essential for the survival of osteocytes; and mice lacking Cx43 in these cells exhibit increased prevalence of osteocyte apoptosis and empty lacunae in cortical bone. Work of several groups for the past few years has unveiled the role of Cx43 on the response of bone cells to a variety of stimuli. Thus, the preservation of the viability of osteoblasts and osteocytes by the anti-osteoporotic drugs bisphosphonates depends on Cx43 expression in vitro and in vivo. This survival effect does not require cell-to-cell communication and is mediated by unopposed hemichannels. Cx43 hemichannels are also required for the release of prostaglandins and ATP by osteocytes induced by mechanical stimulation in vitro. More recent evidence showed that the cAMP-mediated survival effect of parathyroid hormone (PTH) also requires Cx43 expression. Moreover, the hormone does not increase bone mineral content in mice haploinsufficient for Cx43 or lacking Cx43 in osteoblastic cells. Since inhibition of osteoblast apoptosis contributes, at least in part, to bone anabolism by PTH, the lack of response to the hormone might be due to the requirement of Cx43 for the effect of PTH on osteoblast survival. In summary, mounting evidence indicate that Cx43 is a key component of the intracellular machinery responsible for the transduction of signals in the skeleton in response to pharmacologic, hormonal and mechanical stimuli.
Identifiers
22679450PMC3367377W18882757What 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.