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Better Understanding of Cholesterol's Link to Heart Disease
The researchers further found that drugs used to lower cholesterol and inflammation, including statins and rosiglitazone, restore the macrophage network to almost normal, even in mice that don't have the LDL receptors that are considered the usual targets of the drugs. On the other hand, mice lacking single proteins in the network, including APOE and so-called complement proteins of the immune system, have macrophages that look like foam cells even when they aren't loaded with cholesterol. The findings suggest that anything that sends the macrophage network off kilter could promote heart disease, Heinecke said. They also change the way researchers should think about how heart disease is treated. The key may be how to best restore the function of an integrated network rather than to lower cholesterol levels or ratchet individual proteins up or down.
"We propose that the atherogenic actions of cholesterol-loaded macrophages are an emergent property that results when the normal balance of MSRN proteins in microvesicles is perturbed," the researchers conclude. "We further suggest that certain dietary factors or genetic variations can disturb this network, thereby promoting vascular disease. By integrating mouse and human data, we hope to better understand the MSRN's role in foam cell formation, with the long-term goal of identifying therapeutic interventions for targeting networks rather than individual proteins."
Source-Eurekalert
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