Impaired fibrous repair: a possible contributor to XXXX vulnerability in @entity1 with type II diabetes.

@entity1 @entity32 @entity2362 @entity6 @entity1476 @entity731 @entity65
OBJECTIVE: @entity6 ( @entity6 ) type II is increasing rapidly worldwide. @entity1 with @entity6 II have a greater atherosclerotic burden and higher risk of developing @entity65 . @entity32 has been proposed as the main cause for the high risk of @entity731 in @entity6 II. In this study, we compared markers of @entity32 and fibrous repair in plaques from subjects with and without @entity6 II. APPROACH AND RESULTS: Carotid endarterectomy specimens were obtained from 63 @entity1 with and 131 without @entity6 . Plaque structure, connective tissue proteins, inflammatory cells, and markers were analyzed by immunohistochemistry, ELISA, Mesoscale, and Luminex technology. Carotid plaques from @entity6 had lower levels of extracellular matrix proteins, @entity2362 , and collagen, which are critical for plaque stability. Plaques from @entity6 had reduced levels of platelet-derived growth factor and @entity1476 , both important for tissue repair. No differences were observed in inflammatory markers in plaques from @entity6 and nondiabetic @entity1 . CONCLUSION: This study suggests that @entity731 in subjects with @entity6 II are more prone to rupture because of impaired repair responses rather than to @entity32 . Although this study did not have a mechanistic design, our findings suggest that targeting impaired repair responses in carotid plaques may help to increase our understanding of @entity731 development and vulnerability in @entity1 with @entity6 II.
