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HDL from patients with CKD and rabbit (CKD HDL) exhibited blunted antiaggregant properties by interaction with CD36 receptor. Carbonylation by HNE of proteins from HDL was found to be part of this pathologic behavior. Activation of the platelets in response to this binding was through a SRC kinase–mediated pathway. SRC kinase activation resulted with an increase of phosphorylated JNK (pJNK). Native and CKD HDL apo A1 binds SRB1 and inhibits platelet activation.
