Hokkaido University · Medicine
Professor Toshiyuki Nagai's research lab focuses on the pathophysiology of heart failure, with a particular emphasis on inflammatory and fibrotic mechanisms underlying cardiac remodeling in conditions such as dilated cardiomyopathy, myocardial infarction, and pressure-overload hypertrophy. The lab investigates key biomarkers—including corticosteroids, dendritic cells, C-reactive protein, tenascin-C, and erythropoietin—that modulate disease progression and long-term outcomes. Using both clinical patient studies and translational animal models, the lab aims to identify novel therapeutic targets and predictive markers for heart failure. Their work bridges molecular mechanisms with clinical prognosis, contributing to precision medicine in cardiovascular disease.
Figures are computed from collected data and may differ slightly.
Corticosteroid therapy might have a beneficial effect on long-term clinical outcome in CS patients, particularly by reduction of heart failure admission and retarding the progression of LV systolic dysfunction.
Decreased number of DC in human-infarcted myocardial tissue was associated with increased macrophage infiltration, impaired reparative fibrosis, and the development of cardiac rupture after MI. These findings suggest a protective role of DC in post-MI inflammation and the subsequent healing process.
Serum C-reactive protein (CRP) elevation predicts the development of heart failure in patients with hypertension. CRP activates macrophages and enhances oxidative stress. We hypothesize that CRP itself has a pathogenic role in the development of pressure overload-induced cardiac remodeling. Transgenic mice with human CRP overexpression (CRPtg) and nontransgenic littermates (CON) were subjected to transverse aortic constriction (TAC/CRPtg and TAC/CON) or sham operation (Sham/CRPtg and Sham/CON).
Abstract Aim Dilated cardiomyopathy (DCM) has a variety of causes, and no useful approach to predict left ventricular (LV) remodelling and long-term outcome has yet been established. Myocardial tenascin-C (TNC) is known to appear under pathological conditions, possibly to regulate cardiac remodelling. The aim of this study was to clarify the significance of myocardial TNC expression in LV remodelling and the long-term outcome in DCM. Methods and results One hundred and twenty-three consecutive D
A high EPO level predicts long-term worse clinical outcomes in ADHF patients, independent of anaemia and impaired renal function. Anaemia and hypoxia due to severe congestion may synergistically contribute to a high EPO level in high-risk HF patients.
We estimated that the prevalence of HF in Japan was 2.2-3.7% for patients aged ≤74 during the period 2014-2019 using the JMDC database, while the prevalence for patients of all ages was 6.5% using the MDV database.
Increased sIL-2R is associated with worse long-term clinical outcomes accompanied by increased systemic inflammatory activity in CS patients.
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