Kosei Ishimaru
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View article: Deferasirox Targeting Ferroptosis Synergistically Ameliorates Myocardial Ischemia Reperfusion Injury in Conjunction With Cyclosporine A
Deferasirox Targeting Ferroptosis Synergistically Ameliorates Myocardial Ischemia Reperfusion Injury in Conjunction With Cyclosporine A Open
Background Ferroptosis, an iron‐dependent form of regulated cell death, is a major cell death mode in myocardial ischemia reperfusion (I/R) injury, along with mitochondrial permeability transition‐driven necrosis, which is inhibited by cyc…
View article: Doxorubicin causes ferroptosis and cardiotoxicity by intercalating into mitochondrial DNA and disrupting Alas1-dependent heme synthesis
Doxorubicin causes ferroptosis and cardiotoxicity by intercalating into mitochondrial DNA and disrupting Alas1-dependent heme synthesis Open
Clinical use of doxorubicin (DOX) is limited because of its cardiotoxicity, referred to as DOX-induced cardiomyopathy (DIC). Mitochondria-dependent ferroptosis, which is triggered by iron overload and excessive lipid peroxidation, plays a …
View article: Excessive Hypoxia‐Inducible Factor‐1α Expression Induces Cardiac Rupture via p53‐Dependent Apoptosis After Myocardial Infarction
Excessive Hypoxia‐Inducible Factor‐1α Expression Induces Cardiac Rupture via p53‐Dependent Apoptosis After Myocardial Infarction Open
Background Apoptosis plays a pivotal role in cardiac rupture after myocardial infarction (MI), and p53 is a key molecule in apoptosis during cardiac rupture. Hif‐1α (hypoxia‐inducible factor‐1α), upregulated under hypoxia, is a known p53 i…