Lipoprotein lipase: Biosynthesis, regulatory factors, and its role in atherosclerosis and other diseases
Lipoprotein lipase (LPL) is a rate-limiting enzyme that catalyzes hydrolysis of the triglyceride (TG) core of circulating TG-rich lipoproteins including chylomicrons (CM), low-density lipoproteins (LDL) and very low-density lipoproteins (VLDL). A variety of parenchymal cells can synthesize and secre...
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Veröffentlicht in: | Clinica chimica acta 2018-05, Vol.480, p.126-137 |
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Sprache: | eng |
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Zusammenfassung: | Lipoprotein lipase (LPL) is a rate-limiting enzyme that catalyzes hydrolysis of the triglyceride (TG) core of circulating TG-rich lipoproteins including chylomicrons (CM), low-density lipoproteins (LDL) and very low-density lipoproteins (VLDL). A variety of parenchymal cells can synthesize and secrete LPL. Recent studies have demonstrated that complicated processes are involved in LPL biosynthesis, secretion and transport. The enzyme activity of LPL is regulated by many factors, such as apolipoproteins, angiopoietins, hormones and miRNAs. In this article, we also reviewed the roles of LPL in atherosclerosis, coronary heart disease, cerebrovascular accident, Alzheimer disease and chronic lymphocytic leukemia. LPL in different tissues exerts differential physiological functions. The role of LPL in atherosclerosis is still controversial as reported in the literature. Here, we focused on the properties of LPL derived from macrophages, endothelial cells and smooth muscle cells in the vascular wall. We also explore the existence of crosstalk between LPL and those cells when the molecule mainly plays a proatherogenic role. This review will provide insightful knowledge of LPL and open new therapeutic perspectives.
•We have reviewed these complicated processes involved in biosynthesis, secretion, and transportation of LPL.•We explored the relationship of LPL and macrophages, endothelial cells, and vascular smooth muscle cells.•We reviewed its role of LPL in Atherosclerosis and other diseases. |
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ISSN: | 0009-8981 1873-3492 |
DOI: | 10.1016/j.cca.2018.02.006 |