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Hiroaki Shimokawa

Researcher at Tohoku University

Publications -  976
Citations -  56856

Hiroaki Shimokawa is an academic researcher from Tohoku University. The author has contributed to research in topics: Heart failure & Endothelium. The author has an hindex of 111, co-authored 949 publications receiving 48822 citations. Previous affiliations of Hiroaki Shimokawa include University of Nebraska Medical Center & Nagoya University.

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Inflammatory cytokines cause coronary arteriosclerosis-like changes and alterations in the smooth-muscle phenotypes in pigs.

TL;DR: Results indicate that inflammatory cytokines all have a similar ability to induce coronary arteriosclerosis-like changes and hyperconstrictive responses, which are associated with alterations in smooth-muscle phenotypes toward dedifferentiation.
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Prognostic impact of nutritional status in asymptomatic patients with cardiac diseases: a report from the CHART-2 Study.

TL;DR: In this paper, the authors evaluated the impact of nutrition, using the controlling nutritional status (CONUT) score, calculated by the serum albumin and total cholesterol levels, and lymphocyte number, in 3,421 stage B patients from the Tohoku District-2 Study.
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Matrix metalloproteinases are involved in mechanical stretch-induced activation of skeletal muscle satellite cells.

TL;DR: Results from these experiments provide strong evidence that MMPs mediate HGF release from the matrix and that this step in the pathway is downstream from NO synthesis.
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Bradykinin-Induced Vasodilation Is Impaired at the Atherosclerotic Site but Is Preserved at the Spastic Site of Human Coronary Arteries In Vivo

TL;DR: It is suggested that bradykinin causes vasodilation of human epicardial coronary arteries in vivo and that bradaykinin-induced endothelium-dependent vasodilated is impaired at the stenotic site but is preserved at the angiographically normal site where endothelia-dependent Vasodilation by acetylcholine is impaired and at the spastic site.
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Basal Release of Nitric Oxide Is Decreased in the Coronary Circulation in Patients With Heart Failure

TL;DR: Findings suggest that basal release of nitric oxide in the coronary circulation is decreased in patients with heart failure, as indicated by vasoconstricting response to L-NMMA.