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Advances in Molecular Research of Cartilage: 2nd Edition
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Advances in Molecular Research of Cartilage: 2nd Edition

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 June 2025 | Viewed by 1390

Special Issue Editor

Dr. Laura Mangiavini

E-Mail Website
Guest Editor
Department of Biomedical Sciences for Health, University of Milan, 20133 Milan, Italy
Interests: articular cartilage; cartilage lesions; tissue engineering; cell therapy
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

Articular cartilage is a complex tissue; once damaged, it is not able to regenerate. Hence, articular cartilage repair is still challenging for orthopaedic surgeons. The successful treatment of cartilage lesions is fundamental to avoid the onset of degenerative processes often leading to osteoarthritis. In the earliest stage of cartilage lesions, cell therapy combined with tissue engineering strategies can be effective to promote tissue regeneration and counteract the chronicization of catabolic processes.

This Special Issue welcomes original papers and reviews focused on novel cell therapies or tissue engineering strategies for cartilage regeneration. We accept original manuscripts aimed at basic research and the treatment of both acute and chronic cartilage lesions.

Dr. Laura Mangiavini
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

  • articular cartilage
  • cartilage lesions
  • tissue engineering
  • cell therapy

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Related Special Issue

Published Papers (1 paper)

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Research

17 pages, 6152 KiB  
Article
Loss of CHOP Prevents Joint Degeneration and Pain in a Mouse Model of Pseudoachondroplasia
by Jacqueline T. Hecht, Alka C. Veerisetty, Mohammad G. Hossain, Debabrata Patra, Michele Carrer, Frankie Chiu, Dorde Relic, Paymaan Jafar-nejad and Karen L. Posey
Int. J. Mol. Sci. 2025, 26(1), 16; https://doi.org/10.3390/ijms26010016 - 24 Dec 2024
Viewed by 766
Abstract
Pseudoachondroplasia (PSACH), a severe dwarfing condition characterized by impaired skeletal growth and early joint degeneration, results from mutations in cartilage oligomeric matrix protein (COMP). These mutations disrupt normal protein folding, leading to the accumulation of misfolded COMP in chondrocytes. The MT-COMP mouse is [...] Read more.
Pseudoachondroplasia (PSACH), a severe dwarfing condition characterized by impaired skeletal growth and early joint degeneration, results from mutations in cartilage oligomeric matrix protein (COMP). These mutations disrupt normal protein folding, leading to the accumulation of misfolded COMP in chondrocytes. The MT-COMP mouse is a murine model of PSACH that expresses D469del human COMP in response to doxycycline and replicates the PSACH chondrocyte and clinical pathology. The basis for the mutant-COMP pathology involves endoplasmic reticulum (ER) stress signaling through the PERK/eIF2α/CHOP pathway. C/EBP homologous protein (CHOP), in conjunction with a TNFα inflammatory process, upregulates mTORC1, hindering autophagy clearance of mutant COMP protein. Life-long joint pain/degeneration diminishes quality of life, and treatments other than joint replacements are urgently needed. To assess whether molecules that reduce CHOP activity should be considered as a potential treatment for PSACH, we evaluated MT-COMP mice with 50% CHOP (MT-COMP/CHOP+/−), antisense oligonucleotide (ASO)-mediated CHOP knockdown, and complete CHOP ablation (MT-COMP/CHOP−/−). While earlier studies demonstrated that loss of CHOP in MT-COMP mice reduced intracellular retention, inflammation, and growth plate chondrocyte death, we now show that it did not normalize limb growth. ASO treatment reduced CHOP mRNA by approximately 60%, as measured by RT-qPCR, but did not improve limb length similar to MT-COMP/CHOP+/−. Interestingly, both 50% genetic reduction and complete loss of CHOP alleviated pain, while total ablation of CHOP in MT-COMP mice was necessary to preserve joint health. These results indicate that (1) CHOP reduction therapy is not an effective strategy for improving limb length and (2) pain and chondrocyte pathology are more responsive to intervention than the prevention of joint damage. Full article
(This article belongs to the Special Issue Advances in Molecular Research of Cartilage: 2nd Edition)
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