ArticleBone research2013
Elevated Intracellular Ca(2+) Signals by Oxidative Stress Activate Connexin 43 Hemichannels in Osteocytes.
Article in Bone research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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
21 citing papers in PubMed, 25 citations in OpenAlex.
- Mechanical effects in aging of the musculoskeletal system: Molecular signaling and spatial scale alterations.Journal of orthopaedic translation · 2025Review
- Calcium Regulation of Connexin Hemichannels.International journal of molecular sciences · 2024Review
- Cx43 hemichannels and panx1 channels contribute to ethanol-induced astrocyte dysfunction and damage.Biological research · 2024Article
- The Potential Role of Connexins in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2023Review
- Mechanosensitive piezo1 calcium channel activates connexin 43 hemichannels through PI3K signaling pathway in bone.Cell & bioscience · 2022Article
- Osteocytes regulate bone anabolic response to mechanical loading in male mice via activation of integrin α5.Bone research · 2022Article
- High proportion strontium-doped micro-arc oxidation coatings enhance early osseointegration of titanium in osteoporosis by anti-oxidative stress pathway.Bioactive materials · 2022Article
- Connexin hemichannels regulate redox potential via metabolite exchange and protect lens against cellular oxidative damage.Redox biology · 2021Article
- Connexin Gap Junctions and Hemichannels in Modulating Lens Redox Homeostasis and Oxidative Stress in Cataractogenesis.Antioxidants (Basel, Switzerland) · 2021Review
- Article
- Pulpal upregulation of connexin 43 during pulpitis.Clinical oral investigations · 2021Article
- Intercellular Transmission of Hepatic ER Stress in Obesity Disrupts Systemic Metabolism.Cell metabolism · 2021Article
- Connexin Gap Junctions and Hemichannels Link Oxidative Stress to Skeletal Physiology and Pathology.Current osteoporosis reports · 2021Review
- The Mechanosensory Role of Osteocytes and Implications for Bone Health and Disease States.Frontiers in cell and developmental biology · 2021Review
- Vitamin E Blocks Connexin Hemichannels and Prevents Deleterious Effects of Glucocorticoid Treatment on Skeletal Muscles.International journal of molecular sciences · 2020Article
- Connexin43 Hemichannel Targeting With TAT-Gap19 Alleviates Radiation-Induced Endothelial Cell Damage.Frontiers in pharmacology · 2020Article
- Connexin 43 hemichannels protect bone loss during estrogen deficiency.Bone research · 2019Article
- Inhibitors of connexin and pannexin channels as potential therapeutics.Pharmacology & therapeutics · 2017Review
- Connexins in Cardiovascular and Neurovascular Health and Disease: Pharmacological Implications.Pharmacological reviews · 2017Review
- Inhibition of connexin hemichannels alleviates non-alcoholic steatohepatitis in mice.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Elevated oxidative stress (OS) during aging leads to bone loss. OS increases intracellular Ca(2+) ([Ca(2+)]i), resulting in cellular damage and death. We show earlier that Cx43 hemichannels open in response to OS, which serves as a protective mechanism for osteocytes. However, the underlying mechanism is unknown. Here, we found that treatment with H2O2 increased [Ca(2+)]i in osteocytes with [Ca(2+)]i being primarily derived from an extracellular Ca(2+) source. Hemichannel opening induced by OS was inhibited by the depletion of [Ca(2+)]i with BAPTA-AM, a Ca(2+) chelator, suggesting that [Ca(2+)]i influenced the activity of Cx43 hemichannels. Conversely, blockade of hemichannels had no effect on [Ca(2+)]i. A biotinylation assay showed that cell surface-expressed Cx43 was increased by OS, which could be inhibited by BAPTA-AM, suggesting that [Ca(2+)]i is necessary for Cx43 migration to the cell surface in response to OS. Together, these data suggest that increased hemichannel activity induced by OS was likely to be caused by elevated [Ca(2+)]i through increased Cx43 on the cell surface.
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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.