Authors: Liu, Jingwen; Briggs, Michael R; Kraemer, Fredric B

Source: Future Cardiology, Volume 2, Number 5, September 2006 , pp. 605-612(8)

Publisher: Future Medicine

Abstract:

Reduction in blood levels of low-density lipoprotein (LDL) cholesterol lowers the risk of coronary heart disease. The elucidation of cellular pathways that control LDL-receptor expression through a cholesterol-mediated negative feedback mechanism has provided a crucial molecular basis for the development and clinical applications of statins in the treatment of hypercholesterolemia. The characterization of signaling transduction pathways elicited by cytokine oncostatin M (OM) in liver cells has revealed a novel cellular pathway that activates LDL-receptor transcription independent of intracellular levels of cholesterol and sterol-regulatory element binding proteins. This transcriptional activation is achieved through interactions of the sterol-independent regulatory element of LDL-receptor promoter and transcription factors Egr1 and c/EBPβ, and is dependent upon the activation of the extracellular signal-regulated kinase signaling cascade by OM. In vivo OM administration in hyperlipidemic animals reduces circulating cholesterol and prevents lipid accumulation in the liver. Exploring this sterol-independent cellular pathway may lead to new therapeutic advances.

Keywords: hyperlipidemia; LDL receptor; oncostatin M; sterol-independent regulatory element

Document Type: Research article

DOI: http://dx.doi.org/10.2217/14796678.2.5.605

Publication date: 2006-09-01

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• Future Cardiology reflects the new era of cardiology and highlights new molecular approaches in advancing cardiovascular therapy. The journal publishes clinical research, commentary and therapeutic overviews highlighting optimal therapy and future options and strategies.
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