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Effect of Mitoquinone Treatment on Cardiac Function and Pathophysiology in Pressure Overload‐induced Heart Failure
Author(s) -
Goh Kah Yong,
Wende Adam R,
Soorappan Rajasekaran N.,
Halade Ganesh,
DarleyUsmar Victor,
Jinno Miki,
Prabhu Sumanth D.,
Zhou Lufang
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.59.7
Subject(s) - pressure overload , heart failure , medicine , cardiac function curve , oxidative stress , cardiology , tunel assay , ventricular remodeling , mitochondrion , h&e stain , ejection fraction , chemistry , cardiac hypertrophy , biochemistry , immunohistochemistry
Mitochondrial dysfunction has been implicated in the pathogenesis of heart failure (HF). In particular, emerging studies have indicated that mitochondrial‐derived ROS are involved in calcium dysregulation, ventricular remodeling, cardiac cell death, and metabolic abnormality in failing hearts. Mitoquinone (MitoQ), an antioxidant specifically targeted to mitochondria, has been repeatedly shown beneficial effects in mitochondrial‐related diseases. However, the protective effect of MitoQ in pressure overload HF has not been investigated. We hypothesized that MitoQ treatment improves cardiac function and mitigates pathological remodeling by attenuating mitochondrial‐derived oxidative stress. To test the hypothesis, 8‐week male mice were subject to ascending aortic constriction (AAC) to induce acute pressure overload HF. Cardiac function was assessed with echocardiography. Gravimetric data were collected at the end of the studies. Hematoxylin and eosin (H&E) and picrosirius red (PSR) staining was used to assess the histologic characteristics and TUNEL assay was used to evaluate cardiac cell death. Results showed that one week MitoQ treatment improved fractional shortening and ejection function and reduced the heart mass to tibia length ratio in the AAC mice. In addition, collagen deposition in AAC mice were attenuated by MitoQ treatment. Together, these findings suggest that MitoQ treatment confer protective effect in pressure overload‐induced heart failure in mice.