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Osteoblast Differentiation in Human Health and Disease
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Osteoblast Differentiation in Human 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 May 2026 | Viewed by 1939

Special Issue Editor

Prof. Dr. Younho Han

E-Mail Website
Guest Editor
Department of Oral Pharmacology, College of Dentistry, Wonkwang University, Iksan 54538, Republic of Korea
Interests: osteoblast differentiation; adipocyte differentiation; dental stem cell; drug discovery; phytochemicals; melatonin

Special Issue Information

Dear Colleagues,

Osteoblast differentiation is a fundamental process in bone formation and remodeling, playing a crucial role in maintaining skeletal health throughout life. This complex biological process involves the transformation of mesenchymal stem cells into mature, bone-forming osteoblasts. Recent advancements in molecular biology, genetics, and cellular imaging have significantly enhanced our understanding of the mechanisms governing osteoblast differentiation. However, the dysregulation of this process is implicated in various skeletal disorders, including osteoporosis, osteoarthritis, and rare bone diseases, highlighting its importance in both health and disease states.

This Special Issue aims to provide a comprehensive overview of the latest research on osteoblast differentiation in human health and disease. We welcome original research articles, reviews, and perspectives that explore the molecular mechanisms, signaling pathways, and regulatory factors involved in osteoblast differentiation. Topics of interest include, but are not limited to, the role of transcription factors, epigenetic regulation, microRNAs, and extracellular matrix components in osteoblast differentiation. Additionally, we encourage submissions that investigate the impact of environmental factors, aging, and diseases on this process, as well as potential therapeutic strategies targeting osteoblast differentiation for skeletal disorder.

Prof. Dr. Younho Han
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 250 words) can be sent to the Editorial Office for assessment.

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

  • osteoblast differentiation
  • bone remodeling
  • mesenchymal stem cells
  • skeletal diseases
  • osteogenesis
  • bone mineralization
  • osteoporosis

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Published Papers (2 papers)

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Research

26 pages, 14851 KB  
Article
The Role of Osteoblasts in Phenotypic Variability of Dominant Osteogenesis Imperfecta: Evidence from Patients and Murine Models
by Milena Jovanovic, Apratim Mitra, Chris Stephan, Ka Wai Wong, Sara Talvacchio, Antonella Forlino, Michael To, Kenneth M. Kozloff, Ryan K. Dale and Joan C. Marini
Int. J. Mol. Sci. 2025, 26(23), 11722; https://doi.org/10.3390/ijms262311722 - 3 Dec 2025
Viewed by 257
Abstract
One of the hallmarks of Osteogenesis Imperfecta (OI) is phenotypic variability among individuals with the same mutation. The aim of our study is to investigate the under-explored role of osteoblast differentiation in OI phenotypic variability by using human and murine OI osteoblasts. This [...] Read more.
One of the hallmarks of Osteogenesis Imperfecta (OI) is phenotypic variability among individuals with the same mutation. The aim of our study is to investigate the under-explored role of osteoblast differentiation in OI phenotypic variability by using human and murine OI osteoblasts. This is the first comparative study of osteoblasts from OI patients vs. healthy pediatric controls. We investigated osteoblasts carrying COL1A1 substitutions Gly352Ser and Gly589Ser, each expressed in two unrelated patients differing in phenotypic severity. Osteoblasts from type III OI patients with both mutations deposited significantly less mineral vs. type IV. RNA-Seq showed osteoblasts from type IV OI patients with different mutations had downregulated mitochondrial pathways, while osteoblasts from type III OI patients showed downregulation of extracellular matrix pathways. Puromycin assay demonstrated osteoblast protein synthesis was significantly upregulated in type III vs. type IV OI patients. UPR PERK and BiP were reduced in osteoblasts with Gly352Ser from type III and IV OI patients and in osteoblasts with Gly589Ser from a type III OI patient, while both proteins were increased in Gly589Ser osteoblasts from the type IV patient. Additionally, in a murine comparative study, Col1a1 Gly349Ser, called Brtl Ser, showed a much more severe skeletal phenotype than Brtl Cys. Brtl Ser calvarial osteoblasts had reduced collagen secretion and folding with abnormal dermal collagen fibrils vs. wildtype. Also, Brtl Ser osteoblasts showed condensed actin filaments but a similar mineral deposition as Brtl Cys. Electron microscopy revealed elongated mitochondria with cristae dropout in patient and mutant murine osteoblasts. Our study yielded novel insights highlighting osteoblast differentiation, mineralization, and a potential role of mitochondria in OI pathology and phenotypic variability. Full article
(This article belongs to the Special Issue Osteoblast Differentiation in Human Health and Disease)
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13 pages, 7379 KB  
Article
Berberine Derivative Compound 13 as a Potent Promoter of Osteoblast Differentiation via Akt and PKC Signaling Pathways
by Meiyu Piao, Youn Ho Han and Kwang Youl Lee
Int. J. Mol. Sci. 2025, 26(7), 2984; https://doi.org/10.3390/ijms26072984 - 25 Mar 2025
Viewed by 1343
Abstract
Berberine has been widely studied for its biological functions in various diseases, including cancer, diabetes, and cardiovascular diseases. Nevertheless, structural modifications of berberine have been demonstrated to augment its pharmacological efficacy in specific biological processes, particularly osteogenesis. In this study, we aimed to [...] Read more.
Berberine has been widely studied for its biological functions in various diseases, including cancer, diabetes, and cardiovascular diseases. Nevertheless, structural modifications of berberine have been demonstrated to augment its pharmacological efficacy in specific biological processes, particularly osteogenesis. In this study, we aimed to explore new berberine derivatives with pro-osteogenic activity and molecular mechanisms. Our results demonstrated that compound 13 is the most effective among the tested compounds. Compound 13 significantly enhanced BMP4-induced alkaline phosphatase (ALP) staining and increased the transcriptional activity of osteogenic markers such as ALP, Runt-related gene 2 (Runx2), and Osterix at both the mRNA and protein levels. Furthermore, we found that the Akt and PKC signaling pathways play crucial roles in compound 13-induced osteogenesis via treatment with specific inhibitors. The molecular docking results supported the potential interaction between compound 13 and these kinases. These findings highlighted the regulatory role of compound 13 in osteoblast differentiation via the Akt and PKC signaling pathways. Overall, our study provides compelling evidence that compound 13 is a promising therapeutic candidate for the treatment of osteoporosis, with the potential for further development and optimization to improve bone health and strength. Full article
(This article belongs to the Special Issue Osteoblast Differentiation in Human Health and Disease)
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