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Musculoskeletal Diseases: Advances in Molecular Mechanisms and Therapeutic Approaches

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: 31 October 2025 | Viewed by 648

Special Issue Editor


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Guest Editor
Department of Molecular Medicine, School of Medicine, Kyungpook National University, Daegu 41944, Republic of Korea
Interests: osteoblast/osteoclast differentiation; bone remodeling; bone development and homeostasis; bone metastasis; musculoskeletal diseases
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Special Issue Information

Dear Colleagues,

Musculoskeletal diseases encompass a wide range of pathologic conditions affecting bone, joint, muscle, and connective tissues, impacting individuals of all genders and races. The treatment options for these diseases have significantly advanced in recent decades. However, the molecular mechanisms underlying these conditions remain largely unresolved, and a deeper understanding of their pathophysiology is essential for developing more effective therapies. This Special Issue will highlight new insights and breakthroughs in the molecular mechanisms of musculoskeletal diseases, address persistent challenges, and explore emerging therapeutic approaches, all with the ultimate goal of improving clinical outcomes. We encourage submissions focusing on fundamental molecular pathways, novel therapeutic targets, translational approaches, and innovative methodologies that further our understanding of musculoskeletal pathophysiology.

Prof. Dr. Jung Eun Kim
Guest Editor

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Keywords

  • bone
  • muscle
  • tendon
  • cartilage
  • osteoporosis
  • sarcopenia
  • tendinopathy
  • osteoarthritis
  • musculoskeletal pathophysiology

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Published Papers (1 paper)

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Research

12 pages, 1916 KB  
Article
Effects of Methotrexate and Tofacitinib on Mitochondrial Function and Oxidative Stress in Human Synovial Cells In Vitro
by Valentina Mihaylova, Desislav Tomov, Rositsa Karalilova, Zguro Batalov, Anastas Batalov, Victoria Sarafian and Maria Kazakova
Int. J. Mol. Sci. 2025, 26(17), 8173; https://doi.org/10.3390/ijms26178173 - 22 Aug 2025
Viewed by 433
Abstract
Rheumatoid arthritis (RA) is an autoimmune disease affecting the synovium. Mitochondrial dysfunction is considered a critical factor in the pathogenesis of RA. The aim of the study was to determine the effect of methotrexate and tofacitinib on mitochondrial function and oxidative stress in [...] Read more.
Rheumatoid arthritis (RA) is an autoimmune disease affecting the synovium. Mitochondrial dysfunction is considered a critical factor in the pathogenesis of RA. The aim of the study was to determine the effect of methotrexate and tofacitinib on mitochondrial function and oxidative stress in an in vitro study on the model synovial cell line SW982. TNF-alpha-stimulated SW982 cells, as well as control untreated cells, were incubated with methotrexate and tofacitinib. A metabolic test was performed to assess mitochondrial function. The oxidative stress generated after the application of the therapeutics was determined by a chromatographic analysis. The results obtained showed an increase in ATP levels (p < 0.0001) and a decrease in proton leak (p < 0.0003) after treatment with tofacitinib. The opposite trend was observed—reduced ATP production (p < 0.0096) and increased levels of proton leak (p < 0.0001)—after treatment with methotrexate. A two-fold increase in 8-ISOPGF2A was measured in comparison to TNF-alpha-stimulated and untreated cells. The dynamics of mitochondrial activity and oxidative stress were monitored in a certified RA model cell line after the administration of two different therapeutics. Methotrexate was found to induce mitochondrial dysfunction and oxidative stress in vitro, while tofacitinib partially improved mitochondrial parameters. Full article
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