Ihara Eikichi, Akiho Hirotada, Nakamura Kazuhiko, Turner Sara R, Macdonald Justin A
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.
World J Gastrointest Pathophysiol. 2011 Apr 15;2(2):19-25. doi: 10.4291/wjgp.v2.i2.19.
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.
患有胃肠道(GI)动力障碍相关症状的患者数量正在上升。胃肠道动力障碍伴随着胃肠道平滑肌功能的改变。目前可用的能直接影响胃肠道平滑肌并将改变的平滑肌收缩力恢复正常的药物,在治疗胃肠道动力障碍患者方面并不令人满意。我们最近发现,ERK1/2和p38MAPK信号通路不仅在正常肠道平滑肌的收缩反应中,而且在炎症肠道平滑肌的收缩反应中都起着重要作用。在此,我们讨论ERK1/2和p38MAPK信号通路成为胃肠道动力障碍患者新型治疗药物理想靶点的可能性。