A5088454015- Cardiac electrophysiology and arrhythmias
- Mitochondrial Function and Pathology
- Chemotherapy-induced cardiotoxicity and mitigation
- Ferroptosis and cancer prognosis
- Viral Infections and Immunology Research
- Heart rate and cardiovascular health
- ATP Synthase and ATPases Research
- Cardiac Ischemia and Reperfusion
- Heme Oxygenase-1 and Carbon Monoxide
- Cardiac Structural Anomalies and Repair
- Inflammatory Biomarkers in Disease Prognosis
- Autophagy in Disease and Therapy
- Circular RNAs in diseases
- MicroRNA in disease regulation
- Cardiovascular Issues in Pregnancy
- Cardiovascular Function and Risk Factors
- Cardiac Fibrosis and Remodeling
Kyushu University
2021-2023
Ischemia-reperfusion (I/R) injury is a promising therapeutic target to improve clinical outcomes after acute myocardial infarction. Ferroptosis, triggered by iron overload and excessive lipid peroxides, reportedly involved in I/R injury. However, its significance mechanistic basis remain unclear. Here, we show that glutathione peroxidase 4 (GPx4), key endogenous suppressor of ferroptosis, determines the susceptibility Importantly, ferroptosis major mode cell death injury, distinct from...
Clinical use of doxorubicin (DOX) is limited because its cardiotoxicity, referred to as DOX-induced cardiomyopathy (DIC). Mitochondria-dependent ferroptosis, which triggered by iron overload and excessive lipid peroxidation, plays a pivotal role in the progression DIC. Here, we showed that DOX accumulated mitochondria intercalating into mitochondrial DNA (mtDNA), inducing ferroptosis an mtDNA content-dependent manner. In addition, disrupted heme synthesis decreasing abundance...
Ferroptosis, an iron-dependent form of regulated cell death, is a major death mode in myocardial ischemia reperfusion (I/R) injury, along with mitochondrial permeability transition-driven necrosis, which inhibited by cyclosporine A (CsA). However, therapeutics targeting ferroptosis during I/R injury have not yet been developed. Hence, we aimed to investigate the therapeutic efficacy deferasirox, iron chelator, against hypoxia/reoxygenation-induced cultured cardiomyocytes and injury.
Abstract Doxorubicin (DOX) is an effective anti-cancer agent for various malignancies. Nevertheless, it has a side effect of cardiotoxicity, referred to as doxorubicin-induced cardiomyopathy (DIC), that associated with poorer prognosis. This cardiotoxicity limits the clinical use DOX therapeutic Recently, ferroptosis, form regulated cell death induced by accumulation lipid peroxides, been recognized major pathophysiology DIC. Ethoxyquin lipophilic antioxidant widely used food preservation...
Background Apoptosis plays a pivotal role in cardiac rupture after myocardial infarction (MI), and p53 is key molecule apoptosis during rupture. Hif-1α (hypoxia-inducible factor-1α), upregulated under hypoxia, known inducer. However, the of regulatory mechanisms underlying upregulation, apoptosis, MI unclear. Methods Results We induced mice by ligating left anterior descending artery. expressions were border zone at day 5 MI, accompanied apoptosis. In rat neonatal cardiomyocytes, treatment...
Cardiac autoantibodies (cAAbs) are involved in the progression of adverse cardiac remodeling heart failure (HF). However, our understanding cAAbs HF is limited owing to absence relevant animal models. Herein, we aimed establish and characterize a murine model cAAb-positive after myocardial infarction (MI), thereby facilitating development therapeutics targeting post-MI HF.MI was induced BALB/c mice. Plasma were evaluated using modified Western blot-based methods. Prognosis, function,...