Cholesterol is abundant in atherosclerotic lesions, which become most dangerous when they break apart and plug an arterial passage. Unstable lesions are associated with lots of cellular debris, mostly from dead macrophages. Tabas, along with Bo Feng and colleagues, shows in one article that macrophages die in lesions because cholesterol elicits the unfolded protein response (UPR) in the ER.
Macrophages that were unable to deal with the excess cholesterol they ingested had depleted ER calcium stores and...
The Rockefeller University Press
2003
The Rockefeller University Press
2003
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