The University of Tokyo · Medicine
Professor Yasutomi Higashikuni's research lab focuses on cardiac pathophysiology, particularly the molecular and cellular mechanisms underlying heart failure, hypertrophy, and post-myocardial infarction repair. The lab investigates key pathways involving innate immunity (e.g., TLR2 and HSP70), endothelial function, and transporter proteins such as BCRP1/ABCG2 in regulating cardiac adaptation and vascular integrity. Current research also explores the impact of systemic diseases—like COVID-19—on cardiovascular outcomes, emphasizing immune modulation and microvascular dysfunction.
Figures are computed from collected data and may differ slightly.
Cardiac inflammation and hypertrophy are regulated by heart-brain interaction. Controlling neural signals might be important for the treatment of hypertensive heart disease.
Our results demonstrate that TLR2-mediated inflammation induced by extracellularly released heat shock protein 70 is essential for adaptive cardiac hypertrophy in response to pressure overload. Thus, modulation of TLR2 signaling in the heart may provide a novel strategy for treating heart failure due to inadequate adaptation to hemodynamic stress.
BCRP1/ABCG2 plays a pivotal role in cardiac repair after MI via modulation of microvascular endothelial cell survival and function.
ABCG2 protects against pressure overload-induced cardiac hypertrophy and heart failure by promoting angiogenesis and antioxidant response.
Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic with a great impact on social and economic activities, as well as public health. In most patients, the symptoms of COVID-19 are a high-grade fever and a dry cough, and spontaneously resolve within ten days. However, in severe cases, COVID-19 leads to atypical bilateral interstitial pneumonia, acute respiratory distress syndrome, and systemic thromboembolism, r
Culprit plaques of patients with the no-reflow phenomenon differ from those in patients without the no-reflow phenomenon.
Culprit plaques with positive remodeling have a large lipid burden, whereas those with negative remodeling contain a large amount of calcium.
In hypertensive subjects, it has been demonstrated that the lower the blood pressure, the lower the incidence of chronic kidney disease (CKD). However, whether this relationship holds true in individuals without hypertension--that is, in individuals with a blood pressure <140/90 mmHg--remains unknown. This study was performed to assess the relationship between blood pressure and CKD in a Japanese population without hypertension. Among 13,007 Japanese participants in a general health screening, 9
We encountered a 59-year-old man with advanced lung cancer with multiple swollen lymph nodes. At autopsy the lung cancer was revealed as giant cell carcinoma. Microscopic examination showed no cancer cells, but there was polyclonal proliferation of plasma cells in the lymph nodes and in the bone marrow. In the kidneys, proliferation of mesangial matrices and mesangial cells was found. This presentation resembled multicentric Castleman's disease (MCD), in which interleukin-6 (IL-6) has a great ro
Culprit plaques of patients with PA were different from those without PA. Plaque composition may play an important role in the occurrence of PA.
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