Atherogenesis on the chopping block.
Endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) are now established features of the atherosclerotic plaque. In this issue, Thorp et al. (2009) provide initial insights into the causative relationship between UPR and the atherosclerotic disease process, specifically linking the proapoptotic mediator CHOP to plaque growth and necrosis.
Gargalovic
Peter S
PS
Bristol-Myers Squibb Company, Research and Development, Pennington, NJ 08534, USA. peter.gargalovic@bms.com
D000818:Animals; D001057:Apolipoproteins E / Q000172:deficiency / Q000235:genetics; D017209:Apoptosis; D050197:Atherosclerosis / Q000378:metabolism / Q000473:pathology*; D002460:Cell Line; D004721:Endoplasmic Reticulum / Q000378:metabolism*; D006801:Humans; D026502:LDL-Receptor Related Proteins; D051379:Mice; D018345:Mice, Knockout; D034741:RNA, Small Interfering / Q000378:metabolism; D011973:Receptors, LDL / Q000172:deficiency / Q000235:genetics; D051742:Transcription Factor CHOP / Q000172:deficiency* / Q000235:genetics / Q000378:metabolism*
D001057:Apolipoproteins E; C497249:DDIT3 protein, human; C497250:Ddit3 protein, mouse; D026502:LDL-Receptor Related Proteins; C116415:Lrp4 protein, mouse; D034741:RNA, Small Interfering; D011973:Receptors, LDL; D051742:Transcription Factor CHOP