Methotrexate treatment improved myocardial structure and function in type 2 diabetes rats by modulating SIRT3-related pathways, diminishing oxidative stress and inflammation.
Does methotrexate mitigate type 2 diabetes-induced myocardial dysfunction in a rat model?
Low-dose methotrexate mitigates diabetes-induced myocardial dysfunction in rats by modulating SIRT3-related metabolic and inflammatory pathways, suggesting potential utility in diabetic cardiomyopathy.
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The current study explored the potential of methotrexate (MTX) to target type 2 diabetes (T2D)-induced immune response and mitigate the associated myocardial dysfunction, focusing on the modulation of SIRT3-related pathways. T2D was induced in Sprague Dawley rats via a high-fat diet and fructose feeding for 30 days, followed by streptozotocin injection (35 mg/kg, i.p). Rats were treated with low doses of MTX (1 & 2 mg/kg) twice weekly for two weeks after diabetes induction. Treatment with MTX improved myocardial structure and decreased serum markers of injury. MTX attenuated oxidative stress, restored antioxidant capacity, suppressed NF-κB-driven inflammation, and reduced TGF-β-mediated fibrotic changes. Notably, MTX upregulated cardiac SIRT3 and PFKFB3 expression while downregulating p53/TIGAR signaling pathways, indicating an improvement in T2D-induced glycolytic disruption and reduced apoptosis. Conclusively, MTX mitigates T2D-induced myocardial dysfunction by modulating SIRT3-related metabolic and inflammatory signaling pathways, highlighting its potential as a low-cost therapeutic option for diabetes-associated cardiomyopathy.
Elsayed et al. (Thu,) reported a other. Methotrexate treatment improved myocardial structure and function in type 2 diabetes rats by modulating SIRT3-related pathways, diminishing oxidative stress and inflammation.