The major function of the circulatory system is to deliver oxygen and nutrients to the cells throughout body (Del Re et al., 2019;Kaelin et al., 2016). An insufficient blood supply, if not corrected in time, leads to depletion of oxygen and nutrients to vital organs, resulting in organ failure and death. As we know, coronary artery disease (CAD) and stroke caused by ischemia, a sudden and severe blockage of coronary or brain arteries, are one of the most common causes of death worldwide (Khera & Kathiresan, 2017;Vogel et al., 2019).Every year, an estimation of 720,000 people in the United States is hospitalized with acute coronary syndrome or has fatal coronary heart disease events (Rodriguez & Harrington, 2021).Myocardial infarction (MI) is the most severe manifestation of CAD. Approximately every 40 s, an individual is hospitalized due to myocardial infarction (van Diepen et al., 2017). Reperfusion strategies, including angiography and percutaneous coronary intervention (PCI), are the widely used for CAD and MI patients (Thiele et al., 2018). Also, artery bypass graft surgery is considered to treat MI patients with a large myocardial area at jeopardy or cardiogenic shock (Solo et al., 2019). However, these therapeutic strategies are not suitable for some elder patients with diffuse myocardial infarction. To meet the needs
Myocardial ischemic/reperfusion (MI/R) is a leading cause of cardiovascular disease with high morbidity and mortality. However, the mechanisms underlying pathological reperfusion remain obscure. In this study, we found that dioscin, a natural product, could be a potential candidate for treating MI/R through modulating cardiac dysfunction. Mechanistically, our work revealed that dioscin could suppress the production of reactive oxygen species (ROS) via repressing the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 2 (Nox2) and enhancing the expression of antioxidant enzymes, including superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GPx). These findings indicate that dioscin may be a potential candidate for therapeutic interventions in MI/R injury.
Myocardial infarction is one of the most severe heart diseases, leading to sudden death. Currently, angiography and stenting are widely performed in clinics, yet more effective treatment is still needed. Herein, we presented that dioscin, a natural product, showed protective effect on infarcted hearts via mitochondrial maintenance. Upon dioscin treatment, cardiac dysfunction was alleviated, and remodeling is prevented. Mechanistically, disocin maintains mitochondria function through the maintenance of Kreb's cycle, and suppresion of ROS accumulation. In this way, by targeting mitochondrial dysfunction, dioscin is a potential drug for infarcted hearts.
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