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Goova, M.T., Li, J., Kislinger, T., Qu, W., Lu, Y., Bucciarelli, L.G., Nowygrod, S., Wolf, B.M., Caliste, X., Yan, S.F., Stern, D.M. and Schmidt, A.M. (2001) Blockade of Receptor for Advanced Glycation End-Products Restores Effective Wound Healing in Diabetic Mice. The American Journal of Pathology, 159, 513-525. http://dx.doi.org/10.1016/S0002-9440(10)61723-3

has been cited by the following article:

• TITLE: Effects of AGE Inhibition with Aminoguanidine in a Diabetic db/db Mouse Wound Model

  AUTHORS: Margrete Berdal, Trond Jenssen

  KEYWORDS: Diabetes, Wound, Glycation, Inhibition, Animals

  JOURNAL NAME: Journal of Diabetes Mellitus, Vol.4 No.2, May 6, 2014

  ABSTRACT: Advanced glycation end products (AGEs) react non-enzymatically with tissue proteins to form irreversible structures involved in atherosclerosis, nephropathy, retinopathy, neuropathy, and wound healing. Studies on AGE-inhibitors have demonstrated possible prevention of diabetes complications. The present open label study was conducted on aminoguanidine (AGu), an inhibitor of AGE-formation, to examine potential effects on wound healing in diabetes type 2-like db/db mice during 5 - 6 weeks. The animals were divided into 4 groups: AGu from the day of wounding (day 0) topically and/or systemically in drinking water (1 g/L; group 1, n = 13); AGu 1 g/L in drinking water from 7 weeks prior to day 0 (group 2, n = 21); AGu 5 g/L in drinking water from 9 - 11 weeks prior to day 0 (group 3, n = 6); placebo controls (group 4, n = 8). Results: Glycated hemoglobin (A1C) was significantly lower in group 3 compared to the other groups (P P = 0.01; weight-change, P = 0.04, both for linear trend across groups 4, 2, and 3, respectively). Even so, percentage wound closure was not improved in the AGu-treated groups compared to controls (P ≥ 0.8).