The University of Tokyo · Medicine
Professor Eisuke Amiya's research lab focuses on the pathophysiological mechanisms linking vascular dysfunction, oxidative stress, and autonomic nervous system regulation in cardiovascular diseases. The lab investigates the roles of reactive oxygen species, NADPH oxidase, lipid rafts, and free cholesterol in endothelial dysfunction, particularly in conditions such as hypertension, diabetes, and hypercholesterolemia. A key research direction involves understanding how metabolic and structural alterations in cellular microdomains contribute to atherosclerosis and heart failure. The lab also explores clinical implications, including exercise intolerance in atrial fibrillation and the impact of uric acid metabolism on cardiovascular outcomes.
Figures are computed from collected data and may differ slightly.
Endothelial dysfunction and autonomic nervous system dysfunction are both risk factors for atherosclerosis. There is evidence demonstrating that there is a close interrelationship between these two systems. In hypertension, endothelial dysfunction affects the pathologic process through autonomic nervous pathways, and the pathophysiological process of autonomic neuropathy in diabetes mellitus is closely related with vascular function. However, detailed mechanisms of this interrelationship have no
Reactive oxygen species (ROS) and oxidative stress are closely associated with the development of atherosclerosis, and the most important regulator of ROS production in endothelial cells is NADPH oxidase. Activation of NADPH oxidase requires the assembly of multiple subunits into lipid rafts, which include specific lipid components, including free cholesterol and specific proteins. Disorders of lipid metabolism such as hyperlipidemia affect the cellular lipid components included in rafts, result
Vascular endothelial function is impaired in hypercholesterolemia partly because of injury by modified LDL. In addition to modified LDL, free cholesterol (FC) is thought to play an important role in the development of endothelial dysfunction, although the precise mechanisms remain to be elucidated. The aim of this study was to clarify the mechanisms of endothelial dysfunction induced by an FC-rich environment. Loading cultured human aortic endothelial cells with FC induced the formation of vesic
In NIDCM patients, prolonged QRS duration is a high risk factor for remodeling and unfavorable events. The severity of mitral regurgitation was also a strong risk predictor.
The abnormalities in uric acid concentration are common in a variety of clinical settings. Uric acid, a byproduct of purine metabolism, was influenced by several factors, such as high purine or protein diets, alcohol consumption, conditions with high cell turnover, drugs, renal dysfunction, or enzymatic defects in purine metabolism. Further, the development of hypertension,1 renal dysfunction,2 and cardiovascular events3 have all been linked to an increase in serum uric acid. In the mechanistic
The most outstanding feature of the current case was the rapid decrease of cardiac injury and improvement of cardiac function by strengthening antithyroid therapy, including steroid pulse, without thyroid hormone level normalization. In thyroid storm, various systemic inflammatory reactions have different time courses and among them, the cardiac phenotype emerges in most striking and critical ways.
To investigate the effect of atrial fibrillation (AF) on the oxygen uptake and exercise tolerance, we evaluated cardiopulmonary exercise test (CPET) data in AF patients and heart rate-matched controls with sinus rhythm (cSR) who received ambulatory cardiac rehabilitation. We compared CPET data between AF (<i>N</i> = 27) and cSR patients (<i>N</i> = 106) who had similar HRs at rest and the peak points. Oxygen uptake (VO<sub>2</sub>)/kg and relative O<sub>2</sub> pulse (ml/bpm/kg) at rest and the
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