• Masahiro Ohsawa and Junzo Kamei.
• Department of Pathophysiology and Therapeutics, School of Pharmacy and Pharmaceutical Sciences, Hoshi University, 4-41, Ebara 2-Chome, Shinagawa-Ku, Tokyo 142-8501, Japan.
• Eur. J. Pharmacol. 2010 Oct 10;644(1-3):1-4.

AbstractDiabetic neuropathy is one of the most common complications in diabetes, and hyperalgesia and allodynia are serious symptoms of diabetic neuropathy. There are few therapeutic options available for the treatment of such diabetic painful neuropathy. While several reports have indicated that an abnormality of intracellular signaling molecules is involved in the pathogenesis of diabetic painful neuropathy, agents that affect these intracellular signaling molecules have failed to deliver convincing results in clinical trials. Recently, the small molecular G-protein RhoA has been shown to be involved in the pathogenesis of diabetic nephropathy. RhoA and its downstream kinase Rho kinase (ROCK) have been shown to modulate nociceptive transmission in the spinal cord. In this report, we provide a brief overview of the role of the RhoA/ROCK pathway in diabetic complications. We especially focus on the role of the spinal RhoA/ROCK pathway in the pathogenesis of diabetic painful neuropathy. Findings on the association between the spinal RhoA/ROCK pathway and diabetic painful neuropathy may lead to new strategies for its treatment.Copyright 2010 Elsevier B.V. All rights reserved.

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