ArticleBone2013
Connexin 43 deficiency desensitizes bone to the effects of mechanical unloading through modulation of both arms of bone remodeling.
Article in Bone, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 84 citations in OpenAlex.
- A Systematic Review of Animal Models of Disuse-Induced Bone Loss.Calcified tissue international · 2021Pooled it
- BMP9 attenuates microgravity-related disuse osteoporosis by modulating TGFβ and BMP signaling.NPJ microgravity · 2025Article
- Effects of Occlusal Hypofunction on Osteoclastogenesis Induced by Periodontal Ligament Cells.International journal of dentistry · 2025Article
- The potential key genes within focal adhesion that regulate mesenchymal stem cells osteogenesis or adipogenesis in microgravity related disuse osteoporosis: an integrated analysis.Frontiers in endocrinology · 2025Article
- Activation of connexin hemichannels enhances mechanosensitivity and anabolism in disused and aged bone.JCI insight · 2024Article
- Article
- Genetic variation influences the skeletal response to hindlimb unloading in the eight founder strains of the diversity outbred mouse population.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2024Article
- Connexin 43 in the function and homeostasis of osteocytes: a narrative review.Annals of joint · 2024Review
- Osteocytes Exposed to Titanium Particles Inhibit Osteoblastic Cell Differentiation via Connexin 43.International journal of molecular sciences · 2023Article
- Functional Roles of Connexins and Gap Junctions in Osteo-Chondral Cellular Components.International journal of molecular sciences · 2023Review
- Connexin 43 hemichannels and prostaglandin EFrontiers in cell and developmental biology · 2023Review
- Connexin43 in Musculoskeletal System: New Targets for Development and Disease Progression.Aging and disease · 2022Article
- Connexin 43 Channels in Osteocytes Are Necessary for Bone Mass and Skeletal Muscle Function in Aged Male Mice.International journal of molecular sciences · 2022Article
- Similarities Between Disuse and Age-Induced Bone Loss.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Review
- Osteocytic cells exposed to titanium particles increase sclerostin expression and inhibit osteoblastic cell differentiation mostly via direct cell-to-cell contact.Journal of cellular and molecular medicine · 2022Article
- Mechanical regulation of bone remodeling.Bone research · 2022Review
- Update on the effects of microgravity on the musculoskeletal system.NPJ microgravity · 2021Review
- Bone fracture healing: perspectives according to molecular basis.Journal of bone and mineral metabolism · 2021Review
- The Skeletal Cellular and Molecular Underpinning of the Murine Hindlimb Unloading Model.Frontiers in physiology · 2021Review
- Protective Effects of Controlled Mechanical Loading of Bone in C57BL6/J Mice Subject to Disuse.JBMR plus · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Connexin 43 (Cx43) is a gap junction protein that plays an integral role in the skeletal response to mechanical loading and unloading. In a previous study, we demonstrated preservation of trabecular bone mass and cortical bone formation rate in mice with an osteoblast/osteocyte-selective deficiency of Cx43 (cKO) following mechanical unloading via hindlimb suspension (HLS). In the present study, we sought to define the potential mechanisms underlying this response. Following three weeks of HLS, mRNA levels of Sost were significantly greater in wild-type (WT)-Suspended mice vs. WT-Control, while there was no difference between cKO control and cKO-Suspended. Unloading-induced decreases in P1NP, a serum marker of bone formation, were also attenuated in cKO-Suspended. The proportion of sclerostin-positive osteocytes was significantly lower in cKO-Control vs. WT-Control (-72%, p<0.05), a difference accounted for by the presence of numerous empty lacunae in the cortical bone of cKO vs. WT. Abundant TUNEL staining was present throughout the cortical bone of the tibia and femur, suggesting an apoptotic process. There was no difference in empty lacunae in the trabecular bone of the tibia or femur. Trabecular and cortical osteoclast indices were lower in cKO-Suspended vs. WT-Suspended; however, mRNA levels of the gene encoding RANKL increased similarly in both genotypes. Connexin 43 deficient mice experience attenuated sclerostin-mediated suppression of cortical bone formation and lower cortical osteoclast activity during unloading. Preservation of trabecular bone mass and attenuated osteoclast activity during unloading, despite an apparent lack of effect on osteocyte viability at this site, suggests that an additional mechanism independent of osteocyte apoptosis may also be important. These findings indicate that Cx43 is able to modulate both arms of bone remodeling during unloading.
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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.