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Biomedicines
Special Issues
New Insights into Bone and Cartilage Biology
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New Insights into Bone and Cartilage Biology

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: 30 June 2025 | Viewed by 3338

Special Issue Editor

Dr. Vincent Yuan

E-Mail Website
Guest Editor
Department of Otolaryngology, University of Pittsburgh Medical Center, 600 Grant St, Pittsburgh, PA 15219, USA
Interests: chronic inflammatory diseases; immune-mediated hearing disorders; macrophage and T cell biology; inflammasome activation; biomarkers; therapeutic targets
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Bone and cartilage are dynamic tissues that depend on precisely regulated molecular and cellular processes to maintain their structural integrity and function. Disruptions in these processes can result in debilitating conditions such as osteoporosis and osteoarthritis (OA). This Special Issue will share cutting-edge research articles and comprehensive reviews that investigate the mechanisms driving bone loss, cartilage degeneration, and skeletal disorders, with a focus on the interplay among molecular biology, cellular metabolism, and immune signaling.

Recent advances have underscored the importance of immune pathways, post-translational modifications, and mitochondrial function in skeletal health. Research has identified key regulators, including the vitamin D receptor and circadian genes, that play pivotal roles in osteoblast survival, bone remodeling, and cartilage maintenance. Additionally, insights into inflammatory signaling, acetylation, ubiquitination, and mitochondrial dysfunction have revealed promising targets for innovative therapies.

This Special Issue aims to bring together diverse perspectives on the molecular networks that underpin bone and cartilage biology. Topics of interest include, but are not limited to, mechanisms of skeletal development, immune regulation, mitochondrial dynamics, post-translational modifications, and advancements in skeletal disease therapies. Contributions highlighting novel biomarkers, therapeutic strategies, and translational approaches to the prevention or treatment of osteoporosis, OA, and related disorders are especially encouraged.

By showcasing these groundbreaking insights, we aim to inspire innovative research and foster collaborations that will advance our understanding and treatment of skeletal diseases.

Dr. Vincent Yuan
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. Biomedicines is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). 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 remodeling
  • cartilage degeneration
  • osteoporosis
  • osteoarthritis
  • mitochondrial function
  • protein modifications
  • immune signaling
  • therapeutic strategies

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Published Papers (4 papers)

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Research

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24 pages, 18947 KiB  
Article
Mechanistic Insights into Salvigenin for Glucocorticoid-Induced Femoral Head Osteonecrosis: A Network Pharmacology and Experimental Study
by Zhengjie Zhu, Yujian Zhong, Ruyuan He, Changheng Zhong, Junwen Chen and Hao Peng
Biomedicines 2025, 13(3), 614; https://doi.org/10.3390/biomedicines13030614 - 3 Mar 2025
Viewed by 683
Abstract
Background/Objectives: Glucocorticoid-induced osteonecrosis of the femoral head (GIOFH) is a debilitating condition resulting from impaired bone metabolism and vascular disruption due to prolonged glucocorticoid use. This study aimed to explore the therapeutic potential of salvigenin, a flavonoid with antioxidative and estrogen-like properties, in [...] Read more.
Background/Objectives: Glucocorticoid-induced osteonecrosis of the femoral head (GIOFH) is a debilitating condition resulting from impaired bone metabolism and vascular disruption due to prolonged glucocorticoid use. This study aimed to explore the therapeutic potential of salvigenin, a flavonoid with antioxidative and estrogen-like properties, in alleviating GIOFH by modulating estrogen receptor alpha (ESR1) pathways. Methods: A network pharmacology approach was utilized to identify salvigenin’s potential targets and their association with GIOFH. Protein–protein interaction networks, along with Gene Ontology and KEGG pathway analyses, were conducted to clarify salvigenin’s multi-target mechanisms. Molecular docking and dynamics simulations assessed the interaction between salvigenin and ESR1. Experimental validation included in vitro assays on MG63 cells treated with dexamethasone (Dex) to mimic GIOFH, evaluating oxidative stress, apoptosis, osteogenic differentiation, and ESR1 expression. Results: Network analysis identified ESR1, NOS3, and MMP9 as key hub targets of salvigenin. Molecular docking and dynamics simulations confirmed stable binding of salvigenin to ESR1. Salvigenin significantly reduced Dex-induced oxidative stress and apoptosis in osteoblasts while restoring osteogenic differentiation and ESR1 expression. Functional assays showed improved mineralized nodule formation, ALP activity, and mitochondrial integrity in salvigenin-treated cells. Conclusions: Salvigenin exhibits significant therapeutic potential in addressing GIOFH through ESR1-mediated pathways. These results offer a strong foundation for future translational studies and the development of salvigenin-based therapies for glucocorticoid-induced bone disorders. Full article
(This article belongs to the Special Issue New Insights into Bone and Cartilage Biology)
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20 pages, 13742 KiB  
Article
Functionalized GelMA/CMCS Composite Hydrogel Incorporating Magnesium Phosphate Cement for Bone Regeneration
by Xingyu Wang, Xiping Zhang, Changtian Gong, Jian Yang, Jingteng Chen and Weichun Guo
Biomedicines 2025, 13(2), 257; https://doi.org/10.3390/biomedicines13020257 - 21 Jan 2025
Viewed by 804
Abstract
Background: Bone regeneration remains a challenging issue in tissue engineering. The use of hydrogels as scaffolds for bone tissue repair has gained attention due to their biocompatibility and ability to mimic the extracellular matrix. This study aims to develop a functionalized GelMA/CMCS composite [...] Read more.
Background: Bone regeneration remains a challenging issue in tissue engineering. The use of hydrogels as scaffolds for bone tissue repair has gained attention due to their biocompatibility and ability to mimic the extracellular matrix. This study aims to develop a functionalized GelMA/CMCS composite hydrogel incorporating magnesium phosphate cement (MPC) for enhanced bone regeneration. Methods: These composites were developed by incorporating potassium magnesium phosphate hexahydrate (KMgPO4·6H2O, MPC) powders into methacrylated gelatin/carboxymethyl chitosan (GelMA-C) hydrogels. The material’s mechanical properties, antibacterial performance, and cytocompatibility were evaluated. In vitro experiments involved cell viability and osteogenic differentiation assays using rBMSCs as well as angiogenic potential assays using HUVECs. The hydrogel was also assessed for its potential in promoting bone repair in a rat (Sprague-Dawley) model of bone defect. Results: The developed GelMA-CM composite demonstrated improved mechanical properties, biocompatibility, and osteogenic potential compared to individual GelMA or CMCS hydrogels. Incorporation of MPC facilitated the sustained release of ions which promoted osteogenic differentiation of pre-osteoblasts. In vivo results indicated accelerated bone healing in the rat bone defect model. Conclusions: The functionalized GelMA-CM composite could be a viable candidate for clinical applications in bone regeneration therapies. Full article
(This article belongs to the Special Issue New Insights into Bone and Cartilage Biology)
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Review

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17 pages, 1758 KiB  
Review
Rhythms in Remodeling: Posttranslational Regulation of Bone by the Circadian Clock
by Vincent G. Yuan
Biomedicines 2025, 13(3), 705; https://doi.org/10.3390/biomedicines13030705 - 13 Mar 2025
Viewed by 609
Abstract
The circadian clock is a fundamental timekeeping system that regulates rhythmic biological processes in response to environmental light–dark cycles. In mammals, core clock genes (CLOCK, BMAL1, PER, and CRY) orchestrate these rhythms through transcriptional–translational feedback loops, influencing various physiological functions, including bone remodeling. [...] Read more.
The circadian clock is a fundamental timekeeping system that regulates rhythmic biological processes in response to environmental light–dark cycles. In mammals, core clock genes (CLOCK, BMAL1, PER, and CRY) orchestrate these rhythms through transcriptional–translational feedback loops, influencing various physiological functions, including bone remodeling. Bone homeostasis relies on the coordinated activities of osteoblasts, osteoclasts, and osteocytes, with increasing evidence highlighting the role of circadian regulation in maintaining skeletal integrity. Disruptions in circadian rhythms are linked to bone disorders such as osteoporosis. Posttranslational modifications (PTMs), including phosphorylation, acetylation, and ubiquitination, serve as crucial regulators of both circadian mechanisms and bone metabolism. However, the specific role of PTMs in integrating circadian timing with bone remodeling remains underexplored. This review examines the intersection of circadian regulation and PTMs in bone biology, elucidating their impact on bone cell function and homeostasis. Understanding these interactions may uncover novel therapeutic targets for skeletal diseases associated with circadian disruptions. Full article
(This article belongs to the Special Issue New Insights into Bone and Cartilage Biology)
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18 pages, 1602 KiB  
Review
Prg4 and Osteoarthritis: Functions, Regulatory Factors, and Treatment Strategies
by Peng-Jie Fu, Sheng-Yuan Zheng, Yan Luo, Zhuo-Qun Ren, Zi-Han Li, Ya-Ping Wang and Bang-Bao Lu
Biomedicines 2025, 13(3), 693; https://doi.org/10.3390/biomedicines13030693 - 12 Mar 2025
Viewed by 774
Abstract
Proteoglycan 4 (PRG4), also known as lubricin, plays a critical role in maintaining joint homeostasis by reducing friction between articular cartilage surfaces and preventing cartilage degradation. Its deficiency leads to early-onset osteoarthritis (OA), while overexpression can protect against cartilage degeneration. Beyond its lubricating [...] Read more.
Proteoglycan 4 (PRG4), also known as lubricin, plays a critical role in maintaining joint homeostasis by reducing friction between articular cartilage surfaces and preventing cartilage degradation. Its deficiency leads to early-onset osteoarthritis (OA), while overexpression can protect against cartilage degeneration. Beyond its lubricating properties, PRG4 exerts anti-inflammatory effects by interacting with Toll-like receptors, modulating inflammatory responses within the joint. The expression of Prg4 is regulated by various factors, including mechanical stimuli, inflammatory cytokines, transcription factors such as Creb5 and FoxO, and signaling pathways like TGF-β, EGFR, and Wnt/β-catenin. Therapeutic strategies targeting PRG4 in OA have shown promising results, including recombinant PRG4 protein injections, gene therapies, and small molecules that enhance endogenous Prg4 expression or mimic its function. Further research into the molecular mechanisms regulating Prg4 expression will be essential in developing more effective OA treatments. Understanding the interplay between Prg4 and other signaling pathways could reveal novel therapeutic targets. Additionally, advancements in gene therapy and biomaterials designed to deliver PRG4 in a controlled manner may hold potential for the long-term management of OA, improving patient outcomes and delaying disease progression. Full article
(This article belongs to the Special Issue New Insights into Bone and Cartilage Biology)
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