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Molecular Aspects of Cartilage Biology
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Molecular Aspects of Cartilage Biology

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 October 2025 | Viewed by 3366

Special Issue Editor

Dr. Michela Geminiani

E-Mail Website
Guest Editor
1. Department of Biotechnology Chemistry & Pharmacy, University of Siena, Via A. Moro, 53100 Siena, Italy
2. SienabioACTIVE, University of Siena, Via A. Moro, 53100 Siena, Italy
Interests: rare disease; osteoarticular disorders; antioxidant; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Articular cartilage, which is a highly specialized tissue, consists mainly of a dense extracellular matrix (ECM) comprising type II collagen fibers, proteoglycans, and water; this is alongside the dispersal of its distinctive cell type, chondrocytes, within the ECM. Chondrocytes play a crucial role in maintaining the cartilage matrix by producing and releasing collagen, proteoglycans, and the enzymes involved in cartilage metabolism. The metabolic function of chondrocytes is governed by the mechanical stress experienced by the tissue.

This Special Issue aims to explore cutting-edge advancements in Cartilage Biology, shedding light on the latest research, methodologies, and breakthroughs regarding the structure, function, and regeneration of cartilage tissues. We welcome contributions encompassing molecular mechanisms, chondrocytes interactions, and translational approaches that enhance our comprehension of cartilage-related disorders and potential therapeutic interventions.

Dr. Michela Geminiani
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.

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Keywords

  • cartilage biology
  • tissue regeneration
  • molecular mechanisms
  • chondrocytes
  • cartilage disorders
  • therapeutic interventions
  • biomaterials

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Published Papers (3 papers)

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Research

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12 pages, 1267 KiB  
Article
A Comprehensive In Vitro and In Silico Approach for Targeting 4-Hydroxyphenyl Pyruvate Dioxygenase: Towards New Therapeutics for Alkaptonuria
by Giulia Bernardini, Alfonso Trezza, Elena Petricci, Giulia Romagnoli, Demetra Zambardino, Fabrizio Manetti, Daniela Braconi, Michela Geminiani and Annalisa Santucci
Int. J. Mol. Sci. 2025, 26(7), 3181; https://doi.org/10.3390/ijms26073181 - 29 Mar 2025
Viewed by 347
Abstract
Alkaptonuria (AKU) is an ultra-rare genetic disorder caused by mutations in the homogentisate 1,2-dioxygenase (HGD) gene, leading to the accumulation of homogentisic acid (HGA). Current treatment options are limited, with Nitisinone (Orfadin or NTBC) being the only approved drug. However, its [...] Read more.
Alkaptonuria (AKU) is an ultra-rare genetic disorder caused by mutations in the homogentisate 1,2-dioxygenase (HGD) gene, leading to the accumulation of homogentisic acid (HGA). Current treatment options are limited, with Nitisinone (Orfadin or NTBC) being the only approved drug. However, its long-term use raises concerns due to significant adverse effects, highlighting the urgent need for safer alternatives. AKU manifests with progressive and often painful symptoms, severely impacting patients’ quality of life. Identifying new therapeutic approaches to inhibit 4-hydroxyphenyl pyruvate dioxygenase (4-HPPD) is critical to improving outcomes for AKU patients. In this study, we present a novel integrated in vitro and in silico strategy to assess the residence time of 4-HPPD inhibitors. In particular, we evaluated several features of a set of triketone compounds including their inhibitory efficacy, residence time, and ochronotic pigment accumulation. By means of our integrated approach, we investigated the pharmacokinetic and pharmacodynamics properties of novel 4-HPPD inhibitors and provided a promising foundation for the development of safer and more effective treatments for AKU. Full article
(This article belongs to the Special Issue Molecular Aspects of Cartilage Biology)
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19 pages, 6248 KiB  
Article
An Osteoblast-Specific Enhancer and Subenhancer Cooperatively Regulate Runx2 Expression in Chondrocytes
by Yuki Matsuo, Xin Qin, Takeshi Moriishi, Viviane K. S. Kawata-Matsuura, Hisato Komori, Chiharu Sakane, Suemi Yabuta, Qing Jiang, Hitomi Kaneko, Kosei Ito, Mayo Shigeta, Takaya Abe and Toshihisa Komori
Int. J. Mol. Sci. 2025, 26(4), 1653; https://doi.org/10.3390/ijms26041653 - 14 Feb 2025
Viewed by 504
Abstract
Runx2 is an essential transcription factor for osteoblast differentiation and chondrocyte maturation. The spatiotemporal expression of Runx2 is regulated by enhancers. We previously identified a 1.3 kb osteoblast-specific enhancer; however, mice with this deletion showed no phenotypes. A 0.8 kb conserved region detected [...] Read more.
Runx2 is an essential transcription factor for osteoblast differentiation and chondrocyte maturation. The spatiotemporal expression of Runx2 is regulated by enhancers. We previously identified a 1.3 kb osteoblast-specific enhancer; however, mice with this deletion showed no phenotypes. A 0.8 kb conserved region detected near the 1.3 kb enhancer did not exhibit enhancer activity in reporter assays, whereas four tandem repeats of 452 bp (452 × 4) containing the most conserved region of 0.8 kb induced strong reporter activity in chondrocyte cell lines. However, chondrocytes of enhanced green fluorescent protein (EGFP) reporter mice using 452 × 4 did not express EGFP. When 452 × 4 was combined with the 1.3 kb enhancer, hypertrophic chondrocytes highly expressed EGFP. Moreover, the 0.8 kb region combined with the 1.3 kb enhancer induced EGFP expression in prehypertrophic and hypertrophic chondrocytes. The deletion of both the 1.3 kb enhancer and the 0.8 kb conserved region slightly reduced Runx2 expression in the limbs. However, neither homozygous nor heterozygous deletions in the Runx2+/− background showed phenotypes. The 0.8 kb conserved region itself lacked enhancer activity, but when combined with the 1.3 kb enhancer, EGFP expression was induced in chondrocytes with a similar expression pattern to Runx2. Therefore, the 0.8 kb conserved region has a novel function as a subenhancer. Full article
(This article belongs to the Special Issue Molecular Aspects of Cartilage Biology)
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Review

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13 pages, 1695 KiB  
Review
Prg4-Expressing Chondroprogenitor Cells in the Superficial Zone of Articular Cartilage
by Nadezda Ignatyeva, Nikita Gavrilov, Peter S. Timashev and Ekaterina V. Medvedeva
Int. J. Mol. Sci. 2024, 25(11), 5605; https://doi.org/10.3390/ijms25115605 - 21 May 2024
Cited by 3 | Viewed by 1917
Abstract
Joint-resident chondrogenic precursor cells have become a significant therapeutic option due to the lack of regenerative capacity in articular cartilage. Progenitor cells are located in the superficial zone of the articular cartilage, producing lubricin/Prg4 to decrease friction of cartilage surfaces during joint movement. [...] Read more.
Joint-resident chondrogenic precursor cells have become a significant therapeutic option due to the lack of regenerative capacity in articular cartilage. Progenitor cells are located in the superficial zone of the articular cartilage, producing lubricin/Prg4 to decrease friction of cartilage surfaces during joint movement. Prg4-positive progenitors are crucial in maintaining the joint’s structure and functionality. The disappearance of progenitor cells leads to changes in articular hyaline cartilage over time, subchondral bone abnormalities, and the formation of ectopic ossification. Genetic labeling cell technology has been the main tool used to characterize Prg4-expressing progenitor cells of articular cartilage in vivo through drug injection at different time points. This technology allows for the determination of the origin of progenitor cells and the tracking of their progeny during joint development and cartilage damage. We endeavored to highlight the currently known information about the Prg4-producing cell population in the joint to underline the significance of the role of these cells in the development of articular cartilage and its homeostasis. This review focuses on superficial progenitors in the joint, how they contribute to postnatal articular cartilage formation, their capacity for regeneration, and the consequences of Prg4 deficiency in these cells. We have accumulated information about the Prg4+ cell population of articular cartilage obtained through various elegantly designed experiments using transgenic technologies to identify potential opportunities for further research. Full article
(This article belongs to the Special Issue Molecular Aspects of Cartilage Biology)
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