Editorial
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World J Gastrointest Pathophysiol. Apr 15, 2011; 2(2): 19-25
Published online Apr 15, 2011. doi: 10.4291/wjgp.v2.i2.19
MAPKs represent novel therapeutic targets for gastrointestinal motility disorders
Eikichi Ihara, Hirotada Akiho, Kazuhiko Nakamura, Sara R Turner, Justin A MacDonald
Eikichi Ihara, Hirotada Akiho, Kazuhiko Nakamura, Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan
Sara R Turner, Justin A MacDonald, Smooth Muscle Research Group, Department of Biochemistry & Molecular Biology University of Calgary, Faculty of Medicine, Calgary, Alberta T2N 4Z6, Canada
Author contributions: Ihara E and Turner SR analyzed the literature and wrote the manuscript. Akiho H, Nakamura K and MacDonald JA supervised and coordinated the project.
Supported by the Research Grant from the Canadian Institutes for Health Research, and Partly by an Alberta Innovates–Health Solutions Senior Scholar Award and Canada Research Chair in Smooth Muscle Pathophysiology
Correspondence to: Hirotada Akiho, MD, PhD, Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashiku, Fukuoka 812-8582, Japan. akiho@intmed3.med.kyushu-u.ac.jp
Telephone: +81-92-642-5286 Fax: +81-92-642-5287
Received: September 17, 2010
Revised: January 28, 2011
Accepted: February 4, 2011
Published online: April 15, 2011
Abstract

The number of patients suffering from symptoms associated with gastrointestinal (GI) motility disorders is on the rise. GI motility disorders are accompanied by alteration of gastrointestinal smooth muscle functions. Currently available drugs, which can directly affect gastrointestinal smooth muscle and restore altered smooth muscle contractility to normal, are not satisfactory for treating patients with GI motility disorders. We have recently shown that ERK1/2 and p38MAPK signaling pathways play an important role in the contractile response not only of normal intestinal smooth muscle but also of inflamed intestinal smooth muscle. Here we discuss the possibility that ERK1/2 and p38MAPK signaling pathways represent ideal targets for generation of novel therapeutics for patients with GI motility disorders.

Keywords: Mitogen-activated protein kinase, P38MAPK, ERK1/2, Smooth muscle, Contractile dysfunction