Action of mitoquinone, a mitochondrial antioxidant, on cardiac mitochondrial metabolism after acute myocardial infarction
Name: GEORGIA AZEVÊDO OLIVEIRA TRAICHEL
Publication date: 26/02/2025
Examining board:
Name |
Role |
|---|---|
| AURELIA ARAUJO FERNANDES | Presidente |
| GIRLANDIA ALEXANDRE BRASIL AMORIM | Examinador Externo |
| IVANITA STEFANON | Coorientador |
| MAICON LANDIM VIEIRA | Examinador Interno |
Summary: Ischemic heart disease is one of the leading causes of heart failure (HF), with mitochondria playing a central role in the progression of this condition. Mitochondrial oxidative stress, alterations in cardiac bioenergetic pathways, and the activation of apoptotic signaling in cardiac tissue are key contributors of this process. In this context, identifying therapeutic strategies capable of directly targeting mitochondrial dysfunction is essential. This study aimed to evaluate the effects of mitoquinone (MitoQ) on mitochondrial function in infarcted rats treated for seven days. Male Wistar rats (aged 10 to 12 weeks) were randomly assigned to three groups: Sham, MI and MI MitoQ. Animals underwent surgery for myocardial infarction (MI) induction or a sham surgical procedure. Mitoquinone (MitoQ) treatment was administered in drinking water for seven days. Cardiac function was assessed by echocardiography, and weight data were analysed. As expected, the MI group showed a reduced ejection fraction and right ventricular hypertrophy, effects that were not reversed by the treatment. However, MitoQ attenuated pulmonary congestion. Additionally, the MI group exhibited an approximately 50% reduction in mitochondrial protein yield (YIELD), which was not restored with short-term treatment. Nevertheless, MitoQ improved mitochondrial calcium retention, enhanced mitochondrial coupling and ATP synthesis capacity, optimized complex I function, and reestablished beta-oxidation. Therefore, our findings suggest that MitoQ was effective in mitigating changes associated with mitochondrial dysfunction and may represent a promising complementary therapeutic strategy for ischemic heart disease, potentially supporting cardiac remodeling after infarction.
