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By interacting with lectin-type Ox-LDL receptor-1, Ox-LDL is capable of suppressing the constitutive eNOS expression [107], elevating the expression of adhesion molecules and chemokines in ECs, and inducing macrophage proliferation, collagen production, vascular smooth muscle cell migration, and platelet activation [108]

In the present study, we asked whether the degenerative cascade initiated by NGF withdrawal could be extrapolated to population of neurons dependent on other neurotrophins, with a particular focus on the degenerative processes affecting BDNF-sensitive neurons

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