ArticleBone research2019
Connexin 43 hemichannels protect bone loss during estrogen deficiency.
Article in Bone research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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.
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Who cites it
33 citing papers in PubMed, 46 citations in OpenAlex.
- Piezo1 Activation Rescues Anabolic Response to Mechanical Loading in Aged Bone via Connexin 43 Hemichannels.Aging cell · 2026Article
- Branched‑chain amino acid metabolism and bone metabolism: Implications for osteoporosis pathogenesis and therapeutic strategies (Review).International journal of molecular medicine · 2026Review
- Glucocorticoids Alter Bone Microvascular Barrier via MAPK/Connexin43 Mechanisms.Advanced healthcare materials · 2025Article
- Global, regional, and national burden of low back pain in postmenopausal women from 1990 to 2021: a comprehensive analysis using data from the Global Burden of Disease Study 2021.Frontiers in endocrinology · 2025Article
- Osteocytes function as biomechanical signaling hubs bridging mechanical stress sensing and systemic adaptation.Frontiers in physiology · 2025Review
- Activation of connexin hemichannels enhances mechanosensitivity and anabolism in disused and aged bone.JCI insight · 2024Article
- BIGH3 mediates apoptosis and gap junction failure in osteocytes during renal cell carcinoma bone metastasis progression.Cancer letters · 2024Article
- Connexin hemichannels drive lactation-induced osteocyte acidification and perilacunar-canalicular remodeling.Cell reports · 2024Article
- Connexin 43 in the function and homeostasis of osteocytes: a narrative review.Annals of joint · 2024Review
- Role of Cx43 on the Bone Cell Generation, Function, and Survival.Bioelectricity · 2023Article
- The role of integrin family in bone metabolism and tumor bone metastasis.Cell death discovery · 2023Review
- Highly-purified rapidly expanding clones, RECs, are superior for functional-mitochondrial transfer.Stem cell research & therapy · 2023Article
- The recent progress of endocrine therapy-induced osteoporosis in estrogen-positive breast cancer therapy.Frontiers in oncology · 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
- Osteocytes regulate bone anabolic response to mechanical loading in male mice via activation of integrin α5.Bone research · 2022Article
- Bone remodeling: an operational process ensuring survival and bone mechanical competence.Bone research · 2022Review
- Extracellular Cysteines Are Critical to Form Functional Cx46 Hemichannels.International journal of molecular sciences · 2022Article
- Probucol promotes osteoblasts differentiation and prevents osteoporosis development through reducing oxidative stress.Molecular medicine (Cambridge, Mass.) · 2022Article
- Connexin 43 Hemichannels Regulate Osteoblast to Osteocyte Differentiation.Frontiers in cell and developmental biology · 2022Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Estrogen deficiency in postmenopausal women is a major cause of bone loss, resulting in osteopenia, osteoporosis, and a high risk for bone fracture. Connexin 43 (Cx43) hemichannels (HCs) in osteocytes play an important role in osteocyte viability, bone formation, and remodeling. We showed here that estrogen deficiency reduced Cx43 expression and HC function. To determine if functional HCs protect osteocytes and bone loss during estrogen deficiency, we adopted an ovariectomy model in wild-type (WT) and two transgenic Cx43 mice: R76W (dominant-negative mutant inhibiting only gap junction channels) and Cx43 Δ130-136 (dominant-negative mutant compromising both gap junction channels and HCs). The bone mineral density (BMD), bone structure, and histomorphometric changes of cortical and trabecular bones after ovariectomy were investigated. Our results showed that the Δ130-136 transgenic cohort had greatly decreased vertebral trabecular bone mass compared to WT and R76W mice, associated with a significant increase in the number of apoptotic osteocyte and empty lacunae. Moreover, osteoclast surfaces in trabecular and cortical bones were increased after ovariectomy in the R76W and WT mice, respectively, but not in ∆130-136 mice. These data demonstrate that impairment of Cx43 HCs in osteocytes accelerates vertebral trabecular bone loss and increase in osteocyte apoptosis, and further suggest that Cx43 HCs in osteocytes protect trabecular bone against catabolic effects due to estrogen deficiency.
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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.