scispace - formally typeset
T

Toshihiro Tsuruda

Researcher at University of Miyazaki

Publications -  64
Citations -  1488

Toshihiro Tsuruda is an academic researcher from University of Miyazaki. The author has contributed to research in topics: Adrenomedullin & Angiotensin II. The author has an hindex of 18, co-authored 57 publications receiving 1373 citations. Previous affiliations of Toshihiro Tsuruda include Matsumoto Dental University & Minami Kyushu University.

Papers
More filters
Journal ArticleDOI

Adrenomedullin: A Possible Autocrine or Paracrine Inhibitor of Hypertrophy of Cardiomyocytes

TL;DR: C cultured neonatal rat cardiomyocytes produce and secrete AM, and the secreted AM inhibits the protein synthesis of these cells, suggesting that AM may act on carduomyocytes as an autocrine or a paracrine factor modulating the cardiac growth.
Journal ArticleDOI

Adrenomedullin: a protective factor for blood vessels.

TL;DR: A body of evidence suggests that AM participates in the mechanism against progression of vascular damage and remodeling, thereby alleviating the ischemia of tissues and organs.
Journal ArticleDOI

Adventitial Mast Cells Contribute to Pathogenesis in the Progression of Abdominal Aortic Aneurysm

TL;DR: In this article, the authors carried out histological study of abdominal aortic aneurysm (AAA) tissues of patients, and interventional animal and cell culture experiments to investigate a role of mast cells in the pathogenesis of AAA.
Journal ArticleDOI

An autocrine or a paracrine role of adrenomedullin in modulating cardiac fibroblast growth.

TL;DR: It is suggested that AM has an important role in modulating the growth of cardiac fibroblasts in an autocrine or a paracrine manner and the secreted AM may inhibit proliferation and protein synthesis of these cells.
Journal ArticleDOI

Pressure-independent effects of pharmacological stimulation of soluble guanylate cyclase on fibrosis in pressure-overloaded rat heart.

TL;DR: It is suggested that sGC stimulator BAY 41–2272 might be effective to reduce fibrosis in hypertensive heart disease by attenuating angiotensin II generation through myofibroblast transformation.