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Cells
Special Issues
Molecular Mechanism of Bone Disease
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Molecular Mechanism of Bone Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (20 August 2024) | Viewed by 6727

Special Issue Editors

Dr. Maria Teresa Valenti

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Guest Editor
Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, 37128 Verona, Italy
Interests: bone degenerative diseases; cancer; transcription factors
Special Issues, Collections and Topics in MDPI journals
Dr. Roberta Zerlotin

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Guest Editor
Department of Emergency and Organ Transplantation, Section of Human Anatomy and Histology, University of Bari, 70124 Bari, Italy
Interests: musculoskeletal system; mouse model; osteosarcopenia; musculoskeletal disease; ageing model; genetic engineering; hind limb unloading; surgical mice model; sarcopenia; osteoporosis; osteoarthritis

Special Issue Information

Dear Colleagues,

Skeletal pathologies afflict a considerable number of individuals worldwide, posing a significant socio-economic and healthcare challenge. Diseases impacting the skeletal system can arise from genetic mutations or result from metabolic alterations that compromise bone remodeling. Primary tumors (such as osteosarcoma) and bone metastases further contribute to the array of conditions affecting bone health. Understanding the molecular and cellular mechanisms leading to alterations in cells responsible for skeletal homeostasis, including osteoblasts and osteoclasts, is crucial. This knowledge not only aids in the identification of disease markers but also facilitates the discovery of molecular targets for the development of pharmaceuticals or treatments aimed at enhancing bone health. Moreover, lifestyle factors, such as nutrition and physical activity, play a role in modulating bone remodeling and counteracting degenerative skeletal pathologies.

Therefore, this Special Issue aims to discuss the latest insights into the molecular and cellular aspects associated with skeletal diseases, examining their roles both as outcomes and triggers. The exploration of molecular and cellular targets as prospective therapeutic avenues for averting or mitigating the advancement of these conditions will also be addressed.

We eagerly anticipate and welcome your valuable contributions.

Dr. Maria Teresa Valenti
Dr. Roberta Zerlotin
Guest Editors

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. Cells is an international peer-reviewed open access semimonthly 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 2700 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
  • mesenchymal stem cells
  • transcription factors
  • bone rare diseases
  • skeletal degenerative diseases

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Published Papers (4 papers)

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Research

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19 pages, 10349 KiB  
Article
FGF23 and Cell Stress in SaOS-2 Cells—A Model Reflecting X-Linked Hypophosphatemia Dynamics
by Lisanne Brueck, Sascha Roocke, Veronika Matschke, Annette Richter-Unruh, Katrin Marcus-Alic, Carsten Theiss and Sarah Stahlke
Cells 2024, 13(18), 1515; https://doi.org/10.3390/cells13181515 - 10 Sep 2024
Viewed by 3542
Abstract
Our study investigates the impact of FGF23 overexpression on SaOS-2 cells to elucidate its role in cellular stress and morphology, contributing to the understanding of skeletal pathologies like X-linked hypophosphatemia (XLH). Using transmission electron microscopy and protein analysis (Western blot), we analyzed the [...] Read more.
Our study investigates the impact of FGF23 overexpression on SaOS-2 cells to elucidate its role in cellular stress and morphology, contributing to the understanding of skeletal pathologies like X-linked hypophosphatemia (XLH). Using transmission electron microscopy and protein analysis (Western blot), we analyzed the rough endoplasmic reticulum (rER) and mitochondria in SaOS-2 cells with FGF23 overexpression compared to controls. We found significant morphological changes, including enlarged and elongated rER and mitochondria, with increased contact zones, suggesting enhanced interaction and adaptation to elevated protein synthesis and secretion demands. Additionally, we observed higher apoptosis rates of the cells after 24–72 h in vitro and upregulated proteins associated with ER stress and apoptosis, such as CHOP, XBP1 (spliced and unspliced), GRP94, eIF2α, and BAX. These findings indicate a robust activation of the unfolded protein response (UPR) and apoptotic pathways due to FGF23 overexpression. Our results highlight the critical role of ER and mitochondrial interactions in cellular stress responses and provide new insights into the mechanistic link between FGF23 signaling and cellular homeostasis. In conclusion, our study underscores the importance of analyzing UPR-related pathways in the development of therapeutic strategies for skeletal and systemic diseases and contributes to a broader understanding of diseases like XLH. Full article
(This article belongs to the Special Issue Molecular Mechanism of Bone Disease)
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Review

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26 pages, 752 KiB  
Review
MicroRNAs and RNA-Binding Protein-Based Regulation of Bone Metastasis from Hepatobiliary Cancers and Potential Therapeutic Strategies
by Sharmila Fagoonee and Ralf Weiskirchen
Cells 2024, 13(23), 1935; https://doi.org/10.3390/cells13231935 - 21 Nov 2024
Viewed by 212
Abstract
Hepatobiliary cancers, such as hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), are among the deadliest malignancies worldwide, leading to a significant number of cancer-related deaths. While bone metastases from these cancers are rare, they are highly aggressive and linked to poor prognosis. This review [...] Read more.
Hepatobiliary cancers, such as hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), are among the deadliest malignancies worldwide, leading to a significant number of cancer-related deaths. While bone metastases from these cancers are rare, they are highly aggressive and linked to poor prognosis. This review focuses on RNA-based molecular mechanisms that contribute to bone metastasis from hepatobiliary cancers. Specifically, the role of two key factors, microRNAs (miRNAs) and RNA-binding proteins (RBPs), which have not been extensively studied in the context of HCC and CCA, is discussed. These molecules often exhibit abnormal expression in hepatobiliary tumors, influencing cancer cell spread and metastasis by disrupting bone homeostasis, thereby aiding tumor cell migration and survival in the bone microenvironment. This review also discusses potential therapeutic strategies targeting these RNA-based pathways to reduce bone metastasis and improve patient outcomes. Further research is crucial for developing effective miRNA- and RBP-based diagnostic and prognostic biomarkers and treatments to prevent bone metastases in hepatobiliary cancers. Full article
(This article belongs to the Special Issue Molecular Mechanism of Bone Disease)
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24 pages, 4561 KiB  
Review
Advances in Regenerative Dentistry: A Systematic Review of Harnessing Wnt/β-Catenin in Dentin-Pulp Regeneration
by Mariam Amir, Lakshmi Jeevithan, Maham Barkat, Syeda Habib Fatima, Malalai Khan, Sara Israr, Fatima Naseer, Sarmad Fayyaz, Jeevithan Elango, Wenhui Wu, José Eduardo Maté Sánchez de Val and Saeed Ur Rahman
Cells 2024, 13(13), 1153; https://doi.org/10.3390/cells13131153 - 6 Jul 2024
Viewed by 1405
Abstract
Dentin pulp has a complex function as a major unit in maintaining the vitality of teeth. In this sense, the Wnt/β-Catenin pathway has a vital part in tooth development, maintenance, repair, and regeneration by controlling physiological activities such as growth, differentiation, and migration. [...] Read more.
Dentin pulp has a complex function as a major unit in maintaining the vitality of teeth. In this sense, the Wnt/β-Catenin pathway has a vital part in tooth development, maintenance, repair, and regeneration by controlling physiological activities such as growth, differentiation, and migration. This pathway consists of a network of proteins, such as Wnt signaling molecules, which interact with receptors of targeted cells and play a role in development and adult tissue homeostasis. The Wnt signals are specific spatiotemporally, suggesting its intricate mechanism in development, regulation, repair, and regeneration by the formation of tertiary dentin. This review provides an overview of the recent advances in the Wnt/β-Catenin signaling pathway in dentin and pulp regeneration, how different proteins, molecules, and ligands influence this pathway, either upregulating or silencing it, and how it may be used in the future for clinical dentistry, in vital pulp therapy as an effective treatment for dental caries, as an alternative approach for root canal therapy, and to provide a path for therapeutic and regenerative dentistry. Full article
(This article belongs to the Special Issue Molecular Mechanism of Bone Disease)
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14 pages, 730 KiB  
Review
Exploring the Role of Circular RNA in Bone Biology: A Comprehensive Review
by Maria Teresa Valenti, Roberta Zerlotin, Mattia Cominacini, Silvia Bolognin, Maria Grano and Luca Dalle Carbonare
Cells 2024, 13(12), 999; https://doi.org/10.3390/cells13120999 - 7 Jun 2024
Cited by 1 | Viewed by 1094
Abstract
Circular RNAs (circRNAs) have emerged as pivotal regulators of gene expression with diverse roles in various biological processes. In recent years, research into circRNAs’ involvement in bone biology has gained significant attention, unveiling their potential as novel regulators and biomarkers in bone-related disorders [...] Read more.
Circular RNAs (circRNAs) have emerged as pivotal regulators of gene expression with diverse roles in various biological processes. In recent years, research into circRNAs’ involvement in bone biology has gained significant attention, unveiling their potential as novel regulators and biomarkers in bone-related disorders and diseases. CircRNAs, characterized by their closed-loop structure, exhibit stability and resistance to degradation, underscoring their functional significance. In bone tissue, circRNAs are involved in critical processes such as osteogenic differentiation, osteoclastogenesis, and bone remodeling through intricate molecular mechanisms including microRNA regulation. Dysregulated circRNAs are associated with various bone disorders, suggesting their potential as diagnostic and prognostic biomarkers. The therapeutic targeting of these circRNAs holds promise for addressing bone-related conditions, offering new perspectives for precision medicine. Thus, circRNAs constitute integral components of bone regulatory networks, impacting both physiological bone homeostasis and pathological conditions. This review provides a comprehensive overview of circRNAs in bone biology, emphasizing their regulatory mechanisms, functional implications, and therapeutic potential. Full article
(This article belongs to the Special Issue Molecular Mechanism of Bone Disease)
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