International Journal of Molecular Sciences

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Musculoskeletal Diseases: Advances in Molecular Mechanisms and Therapeutic Approaches

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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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14 pages, 5181 KB

Open AccessArticle

TGFBI Facilitates Myogenesis and Limits Fibrosis in Mouse Skeletal Muscle Regeneration

by Na Rae Park, So-Yeon Jin, Soon-Young Kim, Seung-Hoon Lee, In-San Kim and Jung-Eun Kim

Int. J. Mol. Sci. 2025, 26(18), 9042; https://doi.org/10.3390/ijms26189042 - 17 Sep 2025

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Abstract

Skeletal muscles are essential for movement and support but are vulnerable to injury. Muscle regeneration relies on the extracellular matrix (ECM), which regulates key cellular processes. Transforming growth factor β-induced (TGFBI), an ECM component involved in cell adhesion, migration, and tissue development, has not been investigated in skeletal muscle regeneration. Here, we examined the role of TGFBI using Tgfbi knockout (KO) mice and C2C12 myoblasts. In vitro, C2C12 cells were treated with recombinant TGFBI following snake venom (SV)-induced injury, and myogenic differentiation and fusion were evaluated by quantitative real-time PCR (qRT-PCR) and Western blotting. In vivo, acute muscle injury was induced by SV injection into the tibialis anterior muscles of 12-week-old wild-type and Tgfbi KO mice, with regeneration assessed by histology and qRT-PCR. TGFBI was absent in uninjured muscle and C2C12 cells but was upregulated after injury. Recombinant TGFBI enhanced myogenic differentiation and restored SV-induced downregulation of myogenic and fusion markers. Although phenotypically normal under physiological conditions, Tgfbi KO mice exhibited impaired regeneration, characterized by persistent immature myofibers, elevated inflammatory cytokines, reduced myogenic marker expression, and increased fibrosis. These findings reveal TGFBI as a key regulator of skeletal muscle repair and a potential therapeutic target for muscle-related disorders. Full article

(This article belongs to the Special Issue Musculoskeletal Diseases: Advances in Molecular Mechanisms and Therapeutic Approaches)

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12 pages, 1916 KB

Open AccessArticle

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

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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 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

(This article belongs to the Special Issue Musculoskeletal Diseases: Advances in Molecular Mechanisms and Therapeutic Approaches)

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