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Mitoquinone Ameliorates Pressure Overload-Induced Cardiac Fibrosis And Left Ventricular Dysfunction In Mice, Kah Yong Goh, Li He, Jiajia Song, Miki Jinno, Aaron J. Rogers, Palaniappan Sethu, Ganesh Halade, Rajasekaran N. Soorappan, Xiaoguang Liu, Sumanth D. Prabhu, Victor Darley-Usmar, Adam R. Wende, Lufang Zhou

Internal Medicine Faculty Publications

Increasing evidence indicates that mitochondrial-associated redox signaling contributes to the pathophysiology of heart failure (HF). The mitochondrial-targeted antioxidant, mitoquinone (MitoQ), is capable of modifying mitochondrial signaling and has shown beneficial effects on HF-dependent mitochondrial dysfunction. However, the potential therapeutic impact of MitoQ-based mitochondrial therapies for HF in response to pressure overload is reliant upon demonstration of improved cardiac contractile function and suppression of deleterious cardiac remodeling. Using a new (patho)physiologically relevant model of pressure overload-induced HF we tested the hypothesis that MitoQ is capable of ameliorating cardiac contractile dysfunction and suppressing fibrosis. To test this C57BL/6J mice were subjected to …