Regulation of Bone Homeostasis: Crosstalk Between Osteoblasts and Osteoclasts

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 8 January 2027 | Viewed by 1687

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Guest Editor
Korea Mouse Phenotyping Center (KMPC), Department of Biochemistry and Cell Biology, Cell and Matrix Research Institute, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea
Interests: bone metabolism and homeostasis; osteoblast and osteoclast signaling; vascular calcification and bone-vascular interactions; molecular mechanisms of skeletal diseases; lipid metabolism and bone remodeling

Special Issue Information

Dear Colleagues,

Bone homeostasis is a tightly regulated process governed by the dynamic balance between bone-forming osteoblasts and bone-resorbing osteoclasts. Disruptions in this equilibrium contribute to skeletal disorders such as osteoporosis, osteoarthritis, and vascular calcification. Understanding the molecular and cellular mechanisms that regulate osteoblast–osteoclast interactions is crucial for developing novel therapeutic strategies to treat bone-related diseases. This Special Issue aims to explore the latest advances in bone biology, focusing on signaling pathways, cellular communication, extracellular vesicles, and regulatory mechanisms that maintain bone homeostasis. We welcome original research and review articles on topics, including but not limited to the following research areas: osteoblast–osteoclast crosstalk, the impact of inflammatory and metabolic factors on bone remodeling, and emerging therapeutic targets for bone disorders. Studies investigating the intersection between vascular and skeletal systems are also encouraged. By gathering insights from multidisciplinary approaches—including molecular biology, bioinformatics, genetics, and translational medicine—this Special Issue seeks to provide a comprehensive understanding of the regulatory networks controlling bone metabolism.

Dr. Xiangguo Che
Guest Editor

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Keywords

  • bone homeostasis
  • bone remodeling
  • osteoporosis
  • vascular calcification
  • osteoblast
  • osteoclast
  • signaling pathways
  • cellular communication
  • regulatory mechanisms

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Published Papers (1 paper)

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Research

13 pages, 2192 KB  
Article
The Role of Follistatin-like 1 in the Cross-Talk Among Osteoclastogenesis, Bone Marrow Stromal Cell Migration, and Osteoblastogenesis In Vitro
by Yongxu Piao, Xiangguo Che, Xian Jin, Dong-Kyo Lee, Min Park, Eun-Jung Heo, Jinyoung Oh, Seong-Gon Kim, Dae-Chul Cho, Hyun-Ju Kim and Je-Yong Choi
Biomedicines 2026, 14(3), 555; https://doi.org/10.3390/biomedicines14030555 - 28 Feb 2026
Viewed by 1012
Abstract
Background: Bone remodeling depends on the dynamic balance between osteoclast-mediated bone resorption and osteoblast-mediated bone formation. Follistatin-like 1 (FSTL1) has been reported as an osteoclast-secreted protein that inhibits osteoclast differentiation, but its direct effects on osteoblast differentiation remain unclear. This study aimed [...] Read more.
Background: Bone remodeling depends on the dynamic balance between osteoclast-mediated bone resorption and osteoblast-mediated bone formation. Follistatin-like 1 (FSTL1) has been reported as an osteoclast-secreted protein that inhibits osteoclast differentiation, but its direct effects on osteoblast differentiation remain unclear. This study aimed to determine whether FSTL1 regulates osteoblast differentiation and mesenchymal stem cell migration and characterizes its role in osteoclast-osteoblast cellular cross-talk under in vitro conditions. Methods: Bone marrow-derived macrophages (BMMs) and stromal cells (BMSCs) from mice were used to induce osteoclast and osteoblast differentiation, respectively. Chemotaxis was assessed by Transwell migration, and osteoblast differentiation was evaluated in BMSC and MC3T3-E1 cells using staining, qRT-PCR, Western blotting, and proliferation assays. Results: FSTL1 significantly suppressed osteoclast differentiation and resorptive activity, confirmed by TRAP staining and pit assay, respectively. Expression of osteoclast markers such as NFATc1, TRAP, and DC-STAMP was reduced under FSTL1 treatment. In BMSCs, FSTL1 did not affect proliferation but significantly enhanced chemotaxis. Moreover, FSTL1 promoted osteogenic differentiation and mineralization, as demonstrated by increased ALP activity and Alizarin Red S staining. In MC3T3-E1 pre-osteoblasts, FSTL1 increased cell proliferation and mineralization by MTS and Alizarin Red staining. Key osteogenic markers, including Runx2 and osteocalcin, were also upregulated. Conclusions: Osteoclast-derived FSTL1 significantly suppresses osteoclastogenesis and promotes mesenchymal cell chemotaxis and osteogenic differentiation, indicating a role in regulating osteoclast–osteoblast cellular interactions in vitro. Targeting FSTL1 signaling may represent a promising therapeutic strategy for osteoporosis and other disorders of impaired bone remodeling. Full article
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