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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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The role of fibroblast growth factor-2 in the vascular effects of interleukin-1β in porcine coronary arteries in vivo

TL;DR: The results suggest that the vascular effects of IL-1 beta may also be mediated by FGF-2 in the swine model and that chronic treatment with F GF-2 also causes coronary arteriosclerotic changes and vasospastic responses in vivo.
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Extracorporeal Shock Wave Therapy for Digital Ulcers of Systemic Sclerosis: A Phase 2 Pilot Study.

TL;DR: ESWT may be added to standard treatments for indolent digital ulcers of SSc, as an effective and safe method, and the average scores on the HAQ, EQ-5D, and PainVision system improved.
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Combination therapy with olmesartan and azelnidipine improves EDHF-mediated responses in diabetic apolipoprotein E-deficient mice.

TL;DR: OLM + AZL may improve the severely impaired EDHF-mediated responses in diabetic ApoE(-/-) mice, in which activation of the endothelial Akt - eNOS pathway may be involved.
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Low-intensity pulsed ultrasound therapy promotes recovery from stroke by enhancing angio-neurogenesis in mice in vivo.

TL;DR: In this paper, low-intensity pulsed ultrasound (LIPUS) therapy was used to improve cognitive dysfunction in mouse models of vascular dementia and Alzheimer's disease, and the results indicated that the LIPUS therapy significantly increased the number of CD31-positive blood vessels in the perifocal lesion and doublecortin (DCX)-positive neurons in the ischemic striatum.
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Protective Role of Myelocytic Nitric Oxide Synthases against Hypoxic Pulmonary Hypertension in Mice.

TL;DR: It is demonstrated that myelocytic n/i/eNOSs play an important protective role in the pathogenesis of PH, suggesting the involvement of immune and inflammatory mechanisms in the exacerbation of hypoxia‐induced PH caused by n/ i/e NOSs−/−‐BM transplantation.