Kyushu University Academic Staff Educational and Research Activities Database
List of Books
Motohiro Nishida Last modified date:2020.01.10

Professor / Department of Translational Pharmaceutical Sciences / Department of Pharmaceutical Health Care and Sciences / Faculty of Pharmaceutical Sciences

1. Nishida M, Sunggip C, Kitajima N & Kurose H, Angiotensin: New Research, Redox regulation of angiotensin receptor signaling in the heart., NOVA Publishers (New York), 2012.03.
2. Nishida M, Ohba M, Nakaya M & Kurose H., Heart Failure: Symptoms, Causes and Treatment Options, NOVA Publishers (New York), Edited by Wright MS. 51-72頁, 2011.03, Structural remodeling of the heart, including myocardial hypertrophy and fibrosis, is a key determinant for the clinical outcome of heart failure. A variety of evidence indicates the importance of neurohumoral factors, such as endothelin-1, angiotensin II, and norepinephrine for the initial phase of the development of cardiac remodeling. These agonists stimulate seven transmembrane spanning receptors that are coupled to heterotrimeric GTP-binding proteins (G proteins) of the Gi, Gq and G12 subfamilies. The pathophysiological roles of each G protein-mediated signaling have been revealed by studies using transgenic and knockout mice. Using specific pharmacological tools to assess the involvement of G protein signaling pathways, we have found that diacylglycerol-activated transient receptor potential canonical (TRPC) channels (TRPC3 and TRPC6), one of the downstream effectors regulated by Gαq, work as a key mediator in the development of cardiac hypertrophy. In contrast, we also revealed that activation of Gα12 family proteins in cardiomyocytes mediates pressure overload-induced cardiac fibrosis. Stimulation of purinergic P2Y6 receptors by extracellular nucleotides released by mechanical stretch is a trigger of Gα12-mediated fibrotic responses of the heart. Although cardiac fibrosis is believed to accompany with Gαq-mediated pathological hypertrophy that eventually results in heart failure, our results clearly show that cardiac fibrosis and hypertrophy are independent processes. These findings will provide a new insight into the molecular mechanisms underlying pathogenesis of heart failure..
3. Mori Y, Itsukaichi Y, Nishida M & Oka H., Pharmacology of Calcium Channel, Kluwer Academic / Plenum Publishers (New York), Kluwer Academic / Plenum Publishers (New York), Edited by McDonough SI.,303-330頁, 2004.06.