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Therapeutic potential of sulfasalazine for sarcopenia: Insights from mouse models and clinical data
Meehee Park1, Seungju Cho1, Seonggyu Choi1
1Mitos Biomedical Institute, Mitos Therapeutics Inc., Daejeon, Republic of Korea.
Abstract:
Sarcopenia, a disease marked by a progressive loss of muscle mass, increases the risks of disability and metabolic disorders, and decreases quality of life. Current therapeutic options are limited. YY1 transcriptional activity is augmented through an interaction with PHF20 at its promoter region, suppressing muscle differentiation. This study screened sulfasalazine, a medication for managing inflammatory bowel diseases (IBD), using the PHF20-YY1 promoter assay in C2C12 myoblasts from an FDA-approved drug library. Sulfasalazine effectively inhibited PHF20-induced YY1 promoter activity (IC50 = 24 μM), reducing YY1 expression and enhancing muscle-specific gene expression. In mouse models of muscle atrophy, sulfasalazine not only enhanced muscle strength and function but also mitigated muscle loss. Clinical data from patients with IBD revealed that those treated with sulfasalazine had a significantly higher TPI (total psoas index), used as a muscle mass marker, suggesting enhanced muscle preservation. In conclusion, this study suggests the potential for repurposing sulfasalazine to manage sarcopenia, especially associated with IBD.
Insights
Sulfasalazine, an inflammatory bowel disease drug, shows promise in treating sarcopenia by inhibiting muscle loss. This study found it improved muscle strength and mass in animal models and patients.
Area of Science:
- Biomedical Science
- Pharmacology
- Muscle Biology
Background:
- Sarcopenia, characterized by progressive muscle mass loss, leads to disability and reduced quality of life, with limited therapeutic options.
- YY1 transcriptional activity, when enhanced by PHF20, suppresses muscle differentiation, contributing to sarcopenia.
- Existing treatments for sarcopenia are insufficient, necessitating novel therapeutic strategies.
Purpose of the Study:
- To screen FDA-approved drugs for potential sarcopenia treatments.
- To investigate the efficacy of sulfasalazine in inhibiting PHF20-induced YY1 promoter activity.
- To evaluate sulfasalazine's effects on muscle mass, strength, and function in preclinical and clinical settings.
Main Methods:
- Utilized a PHF20-YY1 promoter assay in C2C12 myoblasts to screen a drug library.
- Assessed sulfasalazine's inhibitory concentration (IC50) on YY1 promoter activity.
- Evaluated sulfasalazine's impact on muscle strength, function, and mass in mouse models and analyzed clinical data from IBD patients.
Main Results:
- Sulfasalazine demonstrated significant inhibition of PHF20-induced YY1 promoter activity (IC50 = 24 μM).
- Treatment reduced YY1 expression and upregulated muscle-specific gene expression.
- Sulfasalazine improved muscle strength and function, mitigating muscle loss in mice and showing higher total psoas index in IBD patients.
Conclusions:
- Sulfasalazine effectively inhibits a key pathway involved in sarcopenia.
- The drug shows potential for repurposing as a therapeutic agent for sarcopenia.
- Sulfasalazine may be particularly beneficial for sarcopenia associated with inflammatory bowel disease.
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