A major constituent of the fatty arterial plaques seen in heart disease may dampen the inflammation that drives the disease. A cholesterol-precursor molecule may be a mediator of this suppression.
Atherosclerosis progresses as cholesterol-filled immune cells called macrophage foam cells accumulate in arterial walls. Christopher Glass at the University of California, San Diego, and his colleagues found that in mice fed a high-fat, high-cholesterol diet, these cells were linked to suppression of inflammation. Within the foam cells, desmosterol, an intermediate in the cholesterol biosynthesis pathway, accumulated to significantly higher levels than did other intermediates. Moreover, desmosterol was also abundant in human atherosclerotic lesions. In the mice, desmosterol seemed to suppress genes that promote inflammation during foam-cell formation.
Synthetic formulations of desmosterol might intervene in cardiovascular disease, the authors suggest.
Cell 151, 138–152 (2012) http://dx.doi.org/10.1016/j.cell.2012.06.054