# Emerging concepts in osteoarthritis and musculoskeletal diseases: Insights from the University of Debrecen Musculoskeletal Symposium 2025

**Authors:** Patrik Kovács, Judit Vágó, Ali Mobasheri, Zsuzsa Jenei-Lanzl, Frank Zaucke, Henning Madry, László Csernoch, Zoltán Szekanecz, Zsuzsa Szondy, Árpád Szöőr, Istvan Szatmari, Tamás Oláh, Csaba Matta

PMC · DOI: 10.1016/j.ocarto.2025.100728 · 2025-12-11

## TL;DR

The 2025 University of Debrecen Musculoskeletal Symposium explored new insights into osteoarthritis and related diseases, emphasizing interdisciplinary research and potential therapies.

## Contribution

The symposium highlighted novel ECM proteomics findings and emerging therapies like GDF6 and CRISPR for musculoskeletal regeneration.

## Key findings

- ECM degradation fragments identified as potential OA drivers and therapeutic targets.
- GDF6 and CRISPR approaches shown to aid cartilage and disc repair.
- Chronic stress and immune modulation mechanisms linked to OA progression.

## Abstract

To highlight the key translational advances and interdisciplinary discussions from the 2025 University of Debrecen Musculoskeletal Symposium (UD-MUSK), focusing on osteoarthritis (OA) and related musculoskeletal (MSK) diseases.

The UD-MUSK Symposium convened international and local experts for keynote presentations and scientific dialogue spanning OA and MSK disease mechanisms, translational therapies, and tissue regeneration. Core topics included extracellular matrix (ECM) remodelling, cell/gene therapies, animal disease models, chronic stress, autoimmunity, immunotherapies, and muscle and stem cell biology, reflecting the Symposium's broad interdisciplinary spectrum.

ECM proteomics revealed degradation fragments that act as drivers and potential modulators of OA, offering new biomarkers and therapeutic targets. Advances in cell- and gene-based therapies were presented, including the use of growth differentiation factor 6 (GDF6) and CRISPR approaches for cartilage and intervertebral disc repair. Large animal models simulating spatio-temporal changes in human OA, and studies demonstrating chronic stress-accelerated OA via neuroendocrine mechanisms, were highlighted. Novel strategies in immune modulation, such as chimeric antigen receptor (CAR) T cell therapy for autoimmune myopathies, alongside research on muscle regeneration and circadian regulation by mechanical loading, further exemplified the translational breadth of the meeting.

The symposium underscored the value and need of integrating molecular research and disease modeling. Interdisciplinary collaboration continues to enhance understanding of MSK disease mechanisms and supports development of targeted, regenerative therapies with translational potential for OA and related disorders.

## Linked entities

- **Genes:** GDF6 (growth differentiation factor 6) [NCBI Gene 392255]
- **Diseases:** osteoarthritis (MONDO:0005178)

## Full-text entities

- **Genes:** GDF6 (growth differentiation factor 6) [NCBI Gene 392255] {aka BMP-13, BMP13, CDMP2, KFM, KFS, KFS1}
- **Diseases:** autoimmune myopathies (MESH:D009135), musculoskeletal (MSK) diseases (MESH:D009140), OA (MESH:D010003)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12803891/full.md

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Source: https://tomesphere.com/paper/PMC12803891