Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9951221 | European Journal of Vascular and Endovascular Surgery | 2005 | 9 Pages |
Abstract
This wound injury model activates the p38MAPK-signaling cascade in VSMC and causes cell proliferation that can be abrogated by pre-incubation with p38MAPK selective synthetic inhibitors in a time and dose-dependent manner. SB220025 used here for the first time in VSMC reveals itself to be a stronger p38MAPK inhibitor than SB203580 and being a second generation inhibitor may be the preferred drug for novel therapeutic maneuvers.
Keywords
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Authors
T. Jacob, E. Ascher, D. Alapat, Y. Olevskaia, A. Hingorani,