Key result
Cd36-null mice had a delayed time to the formation of occlusive thrombi compared with wild-type mice in a FeCl3-induced carotid artery injury model of diabetes.
The study identifies the AGE-CD36-JNK2 signaling axis as a key mechanism driving platelet hyperreactivity and the prothrombotic phenotype in diabetes.
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Animal data implicate CD36-AGE signaling in diabetic platelet hyperreactivity; leaves open human therapeutic relevance.
Zhu et al. (2012) studied Diabetes mellitus. CD36 deficiency (cd36-null) vs. Wild-type (WT) mice was evaluated on Time to the formation of occlusive thrombi in a FeCl(3)-induced carotid artery injury model. Cd36-null mice had a delayed time to the formation of occlusive thrombi compared with wild-type mice in a FeCl3-induced carotid artery injury model of diabetes.
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