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. Author manuscript; available in PMC: 2009 Jan 5.
Published in final edited form as: Novartis Found Symp. 2007;286:99–203. doi: 10.1002/9780470985571.ch9

Fig. 3. Model of how insulin resistance promotes advanced lesional macrophage apoptosis.

Fig. 3

Macrophage insulin resistance directly activates the UPR, which in turn leads to up-regulation of the SRA. Each of these processes contributes to apoptosis by the two-hit model outlined in Fig. 2. In addition, the up-regulation of the SRA might promote enhanced internalization of lipoprotein-derived cholesterol, which might further activate the UPR in the setting of dysfunctional ACAT and suppressed cholesterol efflux. We are also exploring the possibility that alterations in adipocytokines in the setting of systemic insulin resistance might affect advanced lesional macrophage apoptosis.