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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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Coronary Functional Abnormalities in Patients With Angina and Nonobstructive Coronary Artery Disease.

TL;DR: Results indicate that in patients with angina and nonobstructive CAD, coexistence of epicardial coronary spasm and increased microvascular resistance is associated with worse prognosis, for which Rho-kinase activation may be involved.
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Coronary perivascular fibrosis is associated with impairment of coronary blood flow in patients with non-ischemic heart failure

TL;DR: Coronary perivascular fibrosis is associated with the impairment of coronary blood flow although not associated with interstitial fibrosis or cardiac function, suggesting that it can be a new therapeutic target to improve coronary microcirculation.
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Long-term inhibition of Rho-kinase induces a regression of arteriosclerotic coronary lesions in a porcine model in vivo.

TL;DR: Results indicate that Rho-kinase is substantially involved in constrictive remodeling and vasospastic activity of the arteriosclerotic coronary artery, both of which could be reversed by long-term inhibition of the molecule in vivo.
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Overexpression of eNOS in NTS Causes Hypotension and Bradycardia In Vivo

TL;DR: The results indicate that overexpression of eNOS in the NTS decreases blood pressure, heart rate, and sympathetic nerve activity in conscious rats.
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Role of Monocyte Chemoattractant Protein-1 in Cardiovascular Remodeling Induced by Chronic Blockade of Nitric Oxide Synthesis

TL;DR: It is suggested that MCP-1 is necessary for the development of medial thickening as well as monocyte recruitment in the pathogenesis of fibrosis, in contrast to other factors, such as TGF-&bgr;1.