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Molecular Mechanisms of Bone Development and Differentiation in Health and Disease

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 July 2025 | Viewed by 903

Special Issue Editor

Dr. Cristina Sánchez-De-Diego

E-Mail Website
Guest Editor
Microtechnology, Medicine and Biology (MMB) Lab, Wisconsin Institutes for Medical Research, University of Wisconsin, Madison, WI 53705, USA
Interests: bone; osteocyte differentiation; bone marrow microenvironment; bone metabolism; oxidative stress; cancer research; bone metastasis; microfluidics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue, "Molecular Mechanisms of Bone Development and Differentiation in Health and Disease," provides an in-depth exploration of the molecular pathways and genetic factors crucial to bone formation, growth, and remodeling. Bone is a dynamic tissue that undergoes continuous turnover, balancing between bone formation by osteoblasts and bone resorption by osteoclasts. This balance is essential for maintaining bone health and function. This Special Issue gathers a wide range of research studies that shed light on the complex biological processes governing bone development and differentiation.

Key topics include the role of signaling pathways such as Wnt, BMP, and Notch in regulating osteoblast, osteocyte, and osteoclast activity. This Special Issue also examines how genetic mutations and variations impact these pathways, leading to various bone diseases such as osteoporosis, osteopetrosis, and skeletal dysplasia. Researchers explore how epigenetic factors and microRNAs contribute to the regulation of bone cell differentiation and function.

Additionally, this Special Issue addresses the interplay between systemic factors, such as hormones and nutrients, and local factors within the bone microenvironment that influence bone remodeling. Studies on the molecular mechanisms underlying bone healing and regeneration are also highlighted, offering insights into potential therapeutic approaches for bone repair.

By comprehensively examining these molecular and genetic factors, this Special Issue aims to enhance the understanding of bone biology. This knowledge is crucial for developing innovative strategies to diagnose, prevent, and treat bone-related disorders, ultimately improving bone health and quality of life for individuals affected by these conditions.

Dr. Cristina Sánchez-De-Diego
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • bone differentiation
  • signaling pathways
  • bone diseases
  • bone formation
  • osteoblast
  • osteocyte
  • osteoclast

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Published Papers (2 papers)

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29 pages, 3083 KiB  
Article
Synergistic Crosstalk of PACAP and Notch Signaling Pathways in Bone Development
by Vince Szegeczki, Andrea Pálfi, Csaba Fillér, Barbara Hinnah, Anna Tóth, Lili Sarolta Kovács, Adél Jüngling, Róza Zákány, Dóra Reglődi and Tamás Juhász
Int. J. Mol. Sci. 2025, 26(11), 5088; https://doi.org/10.3390/ijms26115088 - 26 May 2025
Viewed by 167
Abstract
Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide that plays significant regulatory roles in the differentiation of the central nervous system and peripheral organs. A lack of the neuropeptide can lead to abnormalities in long bone development. In callus formation, a possible signaling [...] Read more.
Pituitary adenylate cyclase-activating polypeptide (PACAP) is a neuropeptide that plays significant regulatory roles in the differentiation of the central nervous system and peripheral organs. A lack of the neuropeptide can lead to abnormalities in long bone development. In callus formation, a possible signaling balance shift in PACAP KO mice has been demonstrated, but Notch signalization, with its potential connection with PACAP 1-38, has not been investigated in ossification. Our main goal was to show connections between PACAP and Notch signaling in osteogenesis. Notch signalization showed an elevation in the long bones of PACAP-gene-deficient mice, and it was also elevated during the PACAP 1-38 treatment of UMR-106 and MC3T3-E1 osteogenic cells. Moreover, the inhibition of Notch signaling was compensated by the addition of PACAP 1-38 in vitro. The inorganic and organic matrix production of UMR-106 cells was increased during PACAP 1-38 treatment under the inhibition of Notch signaling. As a possible common target, the expression and nuclear translocation of NFATc1 transcription factor was increased during the disturbance of PACAP and Notch signaling. Our results indicate a possible synergistic regulation during bone formation by PACAP and Notch signalization. The crosstalk between Notch and PACAP signaling pathways highlights the complexity of bone development and homeostasis. Full article
(This article belongs to the Special Issue Molecular Mechanisms of Bone Development and Differentiation in Health and Disease)
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24 pages, 7447 KiB  
Article
Arhgap29 Deficiency Directly Leads to Systemic and Craniofacial Skeletal Abnormalities
by Beibei Zhang, Xiaoyun Pan, Dandan Chi, Yumeng Wang, Wenyan Ruan, Jian Ma, Xiaohong Duan and Yongqing Huang
Int. J. Mol. Sci. 2025, 26(10), 4647; https://doi.org/10.3390/ijms26104647 - 13 May 2025
Viewed by 335
Abstract
The Arhgap29 gene encodes Rho-GTPase-activating protein 29 (Arhgap29), which plays a crucial role in embryonic tissue development. Mutations in the Arhgap29 gene are significantly associated with non-syndromic cleft lip and palate (NSCL/P). Our study demonstrated that the deletion of Arhgap29 leads [...] Read more.
The Arhgap29 gene encodes Rho-GTPase-activating protein 29 (Arhgap29), which plays a crucial role in embryonic tissue development. Mutations in the Arhgap29 gene are significantly associated with non-syndromic cleft lip and palate (NSCL/P). Our study demonstrated that the deletion of Arhgap29 leads to syndromic cleft lip and palate (SCL/P) characteristics in mice, where, in addition to cleft palate, the mice exhibit craniofacial and systemic skeletal abnormalities. However, the mechanisms underlying these skeletal abnormalities remain unclear. Through micro-CT imaging, histological analysis, and transcriptomic methods, we discovered that the knockout of Arhgap29 delays the fusion of Meckel’s cartilage, widens cranial sutures, reduces bone quality, and alters the expression of osteoblasts and osteoclasts in the mandible. Digit defects, including ectrodactyly and impaired endochondral ossification, were also observed. Immunohistochemical analysis demonstrated the expression of Arhgap29 in both osteoblasts and osteoclasts, indicating its dual role in maintaining matrix homeostasis and regulating bone resorption equilibrium. Transcriptomic analysis revealed disrupted calcium and MAPK signaling pathways, while in vitro studies demonstrated impaired osteogenesis in Arhgap29-deficient calvarial cells, mirroring the in vivo defects. Furthermore, spatial transcriptomics linked the loss of Arhgap29 to defective bone differentiation and protein synthesis. Our findings underscore the critical role of Arhgap29 in the development of the mandible and digits, suggesting its potential as a pathogenic gene associated with syndromic cleft lip and palate (SCL/P). Full article
(This article belongs to the Special Issue Molecular Mechanisms of Bone Development and Differentiation in Health and Disease)
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