ArticleInternational journal of molecular sciences2022
Connexin 43 Channels in Osteocytes Are Necessary for Bone Mass and Skeletal Muscle Function in Aged Male Mice.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 18 citations in OpenAlex.
- Bone Aging and Glycative Stress: Convergent and Divergent Mechanisms Driving Skeletal Deterioration.Cells · 2026Review
- From force to resorption: mechanotransduction, osteoclasts, prevention.Progress in orthodontics · 2026Review
- Pathological changes and therapeutic strategies for sarcopenia.EFORT open reviews · 2026Review
- Vascular and musculoskeletal interactions: structure, function, and therapeutic strategies for sarcopenia and osteoporosis.MedScience · 2026Review
- Mitochondrion-targeted therapies for diabetic wound healing: from mechanism to therapeutic opportunity.Burns & trauma · 2026Review
- The role of bone-derived factors in bone and muscle communication.Frontiers in endocrinology · 2025Review
- The Role of PGE2 in Age-related Diseases.Current drug targets · 2025Review
- Molecular communication from bone to skeletal muscle: an overview.Frontiers in cell and developmental biology · 2025Review
- Connexin 43 Modulation in Human Chondrocytes, Osteoblasts and Cartilage Explants: Implications for Inflammatory Joint Disorders.International journal of molecular sciences · 2024Article
- Role of Cx43 on the Bone Cell Generation, Function, and Survival.Bioelectricity · 2023Article
- The Multifaceted Effects of Osteocytic TGFβ Signaling on the Skeletal and Extraskeletal Functions of Bone.Current osteoporosis reports · 2023Review
- Novel insights into osteocyte and inter-organ/tissue crosstalk.Frontiers in endocrinology · 2023Review
- Sirtuins mediate mitochondrial quality control mechanisms: a novel therapeutic target for osteoporosis.Frontiers in endocrinology · 2023Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Osteoporosis and sarcopenia (termed "Osteosarcopenia"), the twin-aging diseases, are major contributors to reduced bone mass and muscle weakness in the elderly population. Connexin 43 (Cx43) in osteocytes has been previously reported to play vital roles in bone homeostasis and muscle function in mature mice. The Cx43-formed gap junctions (GJs) and hemichannels (HCs) in osteocytes are important portals for the exchange of small molecules in cell-to-cell and cell-to-extracellular matrix, respectively. However, the roles of Cx43-based GJs and HCs in both bone and muscle aging are still unclear. Here, we used two transgenic mouse models with overexpression of the dominant negative Cx43 mutants primarily in osteocytes driven by the 10-kb Dmp1 promoter, R76W mice (inhibited gap junctions but enhanced hemichannels) and Δ130-136 mice (both gap junction and hemichannels are inhibited), to determine the actions of Cx43-based hemichannels (HCs) and gap junctions (GJs) in the regulation of bone and skeletal muscle from aged mice (18 months) as compared with those from adult mice (10 months). We demonstrated that enhancement of Cx43 HCs reduces bone mass due to increased osteoclast surfaces while the impairment of Cx43 HCs increases osteocyte apoptosis in aged mice caused by reduced PGE
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Registered trials
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