What question did this study set out to answer?

This study aims to investigate the effects of methotrexate on diabetes-induced myocardial dysfunction via SIRT3-related pathways.

January 9, 2026Biomedicine & PharmacotherapyOpen Access

Targeting the underlying immune mechanism of diabetes-induced myocardial dysfunction via modulation of SIRT-3/p53/TIGAR/PFKFB-3 and SIRT-3/NF-κB signaling pathways as a potential controlling strategy

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Key result

Methotrexate improved myocardial structure and function in type 2 diabetes rats, reducing oxidative stress and inflammation while upregulating SIRT3 and PFKFB3 pathways.

Authors

MEMohamed Salah Eldin Elsayed MEMahmoud Elshal MHManar Gamal HelalMansoura University

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Implication

A study demonstrates that methotrexate improves myocardial function in type 2 diabetes, suggesting a new treatment approach.

Key Points

This study aims to investigate the effects of methotrexate on diabetes-induced myocardial dysfunction via SIRT3-related pathways.
Induced type 2 diabetes in Sprague Dawley rats using a high-fat diet and streptozotocin.
Administered methotrexate in low doses twice weekly for two weeks after diabetes induction.
Assessed myocardial structure and serum markers of injury.
Analyzed oxidative stress, antioxidant capacity, and inflammation.
Methotrexate improved myocardial structure and reduced serum markers of injury.
Attenuated oxidative stress and restored antioxidant capacity.
Suppressed NF-κB-driven inflammation and reduced fibrotic changes.
Upregulated cardiac SIRT3 and PFKFB3, while downregulating p53/TIGAR signaling pathways.

Cite This Study

Elsayed et al. (2026) studied this question. Methotrexate improved myocardial structure and function in type 2 diabetes rats, reducing oxidative stress and inflammation while upregulating SIRT3 and PFKFB3 pathways.

synapsesocial.com/papers/69612fd930ef6c21f6853daf https://doi.org/10.1016/j.biopha.2025.118901

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Targeting the underlying immune mechanism of diabetes-induced myocardial dysfunction via modulation of SIRT-3/p53/TIGAR/PFKFB-3 and SIRT-3/NF-κB signaling pathways as a potential controlling strategy

Discussion

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Implication

Key Points

Cite This Study

Targeting the underlying immune mechanism of diabetes-induced myocardial dysfunction via modulation of SIRT-3/p53/TIGAR/PFKFB-3 and SIRT-3/NF-κB signaling pathways as a potential controlling strategy

Discussion

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Implication

Key Points

Cite This Study

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