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Updated: Jun 2, 2026
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Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
Published on: January 10, 2025
TIF1β Promotes Myocardial Ischemia-Reperfusion Injury by Stabilizing TRAF6 through Mediating TRAF6 SUMOylation
Yue Nan1,2, Xu Zhang1,3, Xinping Du2
1First Central Clinical School, Tianjin Medical University.
International Heart Journal
|May 31, 2026
Summary
Myocardial ischemia-reperfusion injury (MIRI) involves elevated TRAF6. TIF1β mediates TRAF6 SUMOylation, enhancing its stability and promoting MIRI by increasing cell apoptosis and inflammation.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Cellular Pathology
Background:
- Myocardial ischemia-reperfusion injury (MIRI) significantly worsens cardiac damage and function.
- Elevated Tumor Necrosis Factor Receptor Associated Factor 6 (TRAF6) expression is observed in MIRI, but its underlying cause remains unclear.
Purpose of the Study:
- To investigate the mechanism behind elevated TRAF6 expression in MIRI.
- To elucidate the role of TRAF6 SUMOylation and its regulators in MIRI pathogenesis.
Main Methods:
- Established MIRI mouse models via LAD occlusion and reperfusion.
- Utilized hypoxia/reoxygenation (H/R) on AC16 cells.
- Assessed molecular changes using HE staining, Evans blue/TTC staining, RT-qPCR, ELISA, Western blot, and Co-IP.
- Evaluated cell viability and apoptosis via CCK-8 and flow cytometry.
Main Results:
- MIRI models exhibited increased TRAF6 and SUMO1 expression.
- TRAF6 protein SUMOylation, mediated by TIF1β, was found to enhance TRAF6 stability and expression.
- TRAF6 overexpression counteracted the protective effects of TIF1β silencing in H/R-induced cells, reducing viability and increasing apoptosis.
Conclusions:
- TIF1β-mediated SUMOylation stabilizes TRAF6 protein, increasing its levels during MIRI.
- This TRAF6 stabilization facilitates MIRI by promoting cell apoptosis and inflammatory responses while inhibiting cell viability.
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