ArticleMediators of inflammation2025
Gut-Bone Axis Mediates Exercise Modality-Dependent Suppression of Inflammatory Osteoclastogenesis in Ovariectomy-Induced Bone Loss.
Article in Mediators of inflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Myokines in exercise‑mediated bone homeostasis: Molecular signaling mechanisms and therapeutic implications for bone disorders (Review).International journal of molecular medicine · 2026Review
- Targeting the gut‑bone axis through exercise: A novel approach to osteoporosis prevention and treatment (Review).International journal of molecular medicine · 2026Review
- The role of gut microbiota-immune-endocrine crosstalk in the pathogenesis of osteoporosis.Frontiers in immunology · 2026Review
- Gut-Bone Axis Mediates Exercise Modality-Dependent Suppression of Inflammatory Osteoclastogenesis in Ovariectomy-Induced Bone Loss.Mediators of inflammation · 2025Article
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Authors and funding
14 authors.
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Abstract
Exercise is crucial for postmenopausal osteoporosis (PMOP) management, yet the comparative efficacy of different exercise modalities and the underlying mechanisms remain unclear. This study investigated the differential effects of distance-matched high-intensity interval training (HIIT) and moderate-intensity continuous exercise (MICE) on ovariectomy (OVX)-induced osteoporosis (OP) in mice. After 12 weeks of training, micro-CT analysis revealed that MICE, but not HIIT, significantly attenuated OVX-induced bone loss and microstructural deterioration. Crucially, only MICE suppressed osteoclastogenesis and reduced proinflammatory factors (interleukin [IL]-6, IL-1β, and tumor necrosis factor-alpha [TNF-α]) expression in the femur, serum, and colon. Mechanistically, MICE uniquely restored gut microbiota (GM) diversity, mitigated dysbiosis, and enhanced intestinal barrier integrity by upregulating the expression of tight junction proteins (TJPs; ZO-1, occludin, and claudin-1), thereby reducing systemic inflammation. In contrast, HIIT failed to ameliorate GM imbalance and intestinal permeability. Our findings demonstrate that the protective effect of MICE on OVX-induced OP is mediated through the gut-bone axis by modulating GM, repairing the intestinal barrier, and suppressing inflammatory osteoclast activation. This study provides novel evidence that the benefits of exercise on PMOP are modality-dependent, highlighting MICE as a superior strategy and offering mechanistic insights for optimizing exercise prescriptions.
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