title: Diabetic atherosclerosis mouse models.
abstract: Coronary heart disease (CHD) due to atherosclerosis is the leading cause of death in the USA, and accelerated CHD has emerged as a leading cause of morbidity and mortality in diabetic patients in the USA and worldwide. This has highlighted the importance and urgency of studying the mechanism of diabetic atherosclerosis and exploring therapeutic options. Due to its unique advantages over other animal models, the mouse is the most used model for studying the mechanism of diabetes-accelerated atherosclerosis and exploring effective therapeutic approaches. In the past decade, several diabetic atherosclerosis mouse models have been established. Currently, however, there is no ideal animal model for diabetic atherosclerosis. To determine the characteristics of the models that more closely resemble human diabetic atherosclerosis disease, this review focuses on the common diabetic atherosclerosis mouse models with respect to the following issues: (1) whether the mice retain diabetic condition; (2) whether the diabetes accelerates atherosclerosis or increases atherogenic inflammation; (3) whether these factors respond to medical interventions. The discussion is aimed at identifying different diabetic mouse models and their features, in order to heighten awareness of the appropriate models that may provide useful tools for studying the mechanism of diabetes-accelerated atherosclerosis and evaluating therapeutic options.
authors.affiliation: Department of Cardiovascular Disease, Merck Research Laboratories, RY 80W-250, 126 East Lincoln Avenue, Rahway, NJ 07065, USA. ken_wu@merck.com
authors.forename: Kenneth K
authors.initials: KK
authors.lastname: Wu
authors.forename: Youming
authors.initials: Y
authors.lastname: Huan
mesh_terms: D000449:Aldehyde Reductase / Q000235:genetics / Q000378:metabolism; D000818:Animals; D001057:Apolipoproteins E / Q000172:deficiency / Q000235:genetics; D050197:Atherosclerosis / Q000139:chemically induced / Q000209:etiology* / Q000235:genetics; D003921:Diabetes Mellitus, Experimental / Q000139:chemically induced / Q000150:complications; D003922:Diabetes Mellitus, Type 1 / Q000139:chemically induced / Q000150:complications* / Q000235:genetics; D003924:Diabetes Mellitus, Type 2 / Q000150:complications* / Q000209:etiology / Q000235:genetics; D003925:Diabetic Angiopathies / Q000139:chemically induced / Q000209:etiology* / Q000235:genetics; D004040:Dietary Carbohydrates / Q000008:administration & dosage; D004041:Dietary Fats / Q000008:administration & dosage; D004195:Disease Models, Animal; D006801:Humans; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D008822:Mice, Transgenic; D011973:Receptors, LDL / Q000172:deficiency / Q000235:genetics; D013311:Streptozocin
chemical_list: D001057:Apolipoproteins E; D004040:Dietary Carbohydrates; D004041:Dietary Fats; D011973:Receptors, LDL; D013311:Streptozocin; D000449:Aldehyde Reductase