Triglyceride lipases and atherosclerosisOlivecrona, Gunilla; Olivecrona, ThomasCurrent Opinion in Lipidology: October 2010 - Volume 21 - Issue 5 - p 409–415 doi: 10.1097/MOL.0b013e32833ded83 Atherosclerosis: cell biology and lipoproteins: Edited by Petri T. Kovanen and Jan Nilsson Abstract Author Information Purpose of review There are strong epidemiologic connections between plasma triglycerides and atherosclerosis. We will consider to what extent this goes back to derangements of the lipoprotein lipase (LPL) system. The roles of hepatic lipase and endothelial lipase will also be touched upon. Recent findings Understanding of LPL action has taken major steps with the discovery of lipase maturation factor 1 as a specific endoplasmic reticulum chaperon needed for proper folding of the lipases, glycosylphosphatidylinositol-anchored HDL-binding protein 1 as an endothelial cell protein needed for transport and binding of LPL and some angiopoietin-like proteins that can modulate LPL activity. Studies of genetic variants continue to support the important roles of the lipases in lipoprotein metabolism and in atherosclerosis. Conclusion There are several ways by which derangement of the lipases may contribute to atherogenesis. Lipase actions are major determinants of plasma lipoprotein patterns. LPL activity must be modulated in relation to the physiological situation (feeding, fasting, exercise, etc.). Fatty acids and monoglycerides generated must be efficiently removed so that they do not endanger the integrity of the endothelium, cause lipotoxic reactions or both. In addition, the lipases may cause binding and endocytosis of lipoprotein particles in the artery wall. Department of Medical Biosciences, Section on Physiological Chemistry, Umeå University, Umeå, Sweden Correspondence to Gunilla Olivecrona, PhD, Department of Medical Biosciences, Section on Physiological Chemistry, Bldg 6 M 3rd floor, Umeå University, SE-90187 Umeå, Sweden Tel: +46 90 7854491; e-mail: email@example.com © 2010 Lippincott Williams & Wilkins, Inc.