A5013361350- Chemotherapy-induced cardiotoxicity and mitigation
- Cardiac Fibrosis and Remodeling
- Takotsubo Cardiomyopathy and Associated Phenomena
- Glycosylation and Glycoproteins Research
- Immune Cell Function and Interaction
- Pleural and Pulmonary Diseases
- Coronary Artery Anomalies
- Liver Disease Diagnosis and Treatment
- Nitric Oxide and Endothelin Effects
- Mitochondrial Function and Pathology
- Neonatal and fetal brain pathology
- Signaling Pathways in Disease
- NF-κB Signaling Pathways
- Occupational and environmental lung diseases
- Cardiovascular Issues in Pregnancy
- Peptidase Inhibition and Analysis
- Cerebrovascular and Carotid Artery Diseases
- Diamond and Carbon-based Materials Research
- Cardiovascular Disease and Adiposity
- Diabetes Treatment and Management
- Kawasaki Disease and Coronary Complications
- interferon and immune responses
- Cardiac Imaging and Diagnostics
- RNA and protein synthesis mechanisms
- Hepatitis B Virus Studies
Kyushu University
1989-2023
Kyushu University Hospital
2017
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...
Mitochondrial DNA (mtDNA)-induced myocardial inflammation is intimately involved in cardiac remodeling. ZBP1 (Z-DNA binding protein 1) a pattern recognition receptor positively regulating response to mtDNA inflammatory cells, fibroblasts, and endothelial cells. However, the role of remodeling remains unclear. The aim this study was elucidate mtDNA-induced cardiomyocytes failing hearts.mtDNA administrated into isolated cardiomyocytes. Myocardial infarctionwas conducted wild type knockout...
Abstract Although several ribosomal protein paralogs are expressed in a tissue-specific manner, how these proteins affect translation and why they required only certain tissues have remained unclear. Here we show that RPL3L, paralog of RPL3 specifically heart skeletal muscle, influences elongation dynamics. Deficiency RPL3L-containing ribosomes RPL3L knockout male mice resulted impaired cardiac contractility. Ribosome occupancy at mRNA codons was found to be altered the RPL3L-deficient...
To clarify the virological differences in patients with chronic hepatitis C virus (HCV) infection and without liver damage, we assessed HCV markers 306 from a rural area of Japan. Genotypes RNA were determined by polymerase chain reaction, levels branched DNA signal-amplification assay. All had undergone annual tests for alanine aminotransferase (ALT) 1986 to 1995. Patients categorized into three groups: group A, 121 (39.5%) normal ALT on all occasions 10 years; B, 127 (41.5%) intermittently...
Abstract Ca 2+ /calmodulin-dependent protein kinase II (CaMKII) and nuclear factor-kappa B (NF-κB) play crucial roles in pathogenesis of doxorubicin (DOX)-induced cardiomyopathy. Their activities are regulated by intracellular . We hypothesized that blockade L-type channel (LTCC) could attenuate DOX-induced cardiomyopathy regulating CaMKII NF-κB. DOX activated NF-κB through their phosphorylation increased cleaved caspase 3 cardiomyocytes. Pharmacological or gene knockdown LTCC nifedipine...
Nox4 (NADPH [Nicotinamide adenine dinucleotide phosphate] oxidase 4) is a major source of oxidative stress and intimately involved in cardiac hypertrophy. DPP (Dipeptidyl peptidase)-4 inhibitor has been reported to regulate expression adipose tissues. However, its effects on hypertrophy are still unclear. We investigated whether DPP-4 could ameliorate by regulating downstream targets. Ang II (Angiotensin II; 1.44 mg/kg per day) or saline was continuously infused into C57BL/6J mice with...
To assess whether coronary spasm affects the progression of atherosclerosis and results in evolution myocardial infarction, role on fine structure conduit arteries was studied morphologically. Göttingen miniature pigs were fed a semisynthetic diet containing 2% cholesterol 1.1% sodium cholate. One month after being this diet, anesthetized endothelium branch left artery denuded using balloon catheter. X-ray irradiation dose 1,500 rad given twice selectively to area denuded, 4 5 months...
Molecular mechanisms mediating cardiac hypertrophy by glucose metabolism are incompletely understood. Hexosamine biosynthesis pathway (HBP), an accessory of glycolysis, is known to be involved in the attachment O-linked N-acetylglucosamine motif (O-GlcNAcylation) proteins, a post-translational modification. We here demonstrate that glutamine-fructose-6-phosphate amidotransferase 2 (GFAT2), critical HBP enzyme, major isoform GFAT heart and increased response several hypertrophic stimuli,...
Doxorubicin (DOX)-induced cardiomyopathy has poor prognosis, and myocardial inflammation is intimately involved in its pathophysiology. The role of invariant natural killer T (iNKT) cells not been fully determined this disease. We here demonstrated that activation iNKT by α-galactosylceramide (GC) attenuated DOX-induced cardiomyocyte death cardiac dysfunction. αGC increased interferon (IFN)-γ phosphorylation signal transducers activators transcription 1 (STAT1) extracellular signal-regulated...
Abstract Background Invariant natural killer T (iNKT) cells orchestrate tissue inflammation via regulating various cytokine productions, especially strongly upregulating interferon (IFN)-γ. Activation of iNKT have been previously reported to exert protective effects against post-infarcted cardiac remodeling and ischemia/reperfusion injury. However, the role has not determined in doxorubicin (DOX)-induced cardiomyopathy. Purpose The purpose this study was examine whether activation by...