Cell cycle and apoptosis genes in atherosclerosis

Leiden Repository

Cell cycle and apoptosis genes in atherosclerosis

Type: Doctoral Thesis
Title: Cell cycle and apoptosis genes in atherosclerosis
Author: Boesten, Lianne Simone Mirjam
Publisher: Dept. of Internal Medicine, Faculty of Medicine / Leiden University Medical Center (LUMC), Leiden University
Issue Date: 2006-03-01
Keywords: Atherosclerosis
Apoptosis
Necrosis
Inflammation
Proliferation
Mouse models
Cell cycle
Retinoblastoma
p53
Tumor Necrosis Factor
Abstract: The work described in this thesis was aimed at identifying the role of cell cycle and apoptosis genes in atherosclerosis. Atherosclerosis is the primary cause of cardiovascular disease, a disorder occurring in the large and medium-sized arteries of the body. Although in the beginning 90s promising lipid lowering therapies predicted a strong reduction in cardiovascular deaths, in westernized societies it is still the underlying cause of about 40% of all deaths, indicating that treatment of atherosclerosis goes beyond lipid lowering solely. In addition to lipids, continuous cell growth (cell cycle) and cell death (i.e. apoptosis and necrosis) processes play a central role in the development of atherosclerosis. To investigate the role of several cell cycle and apoptosis genes (i.e. p53, Rb and Mdm2) in atherosclerosis we generated and characterized several mouse models based on site-specific recombinase (SSR) technology. The studies described in this thesis show that next to therapies aiming at lifestyle interventions, lipid therapies and regulation of inflammation, targeting cell cycle and apoptosis genes on lesional or cellular level might prove the most effective way to reduce the burden of atherosclerosis.
Description: Promotor: L.M. Havekes, Co-promotores: B.J.M. van Vlijmen, M.P.J. de Winther
With summary in Dutch
Faculty: LUMC
Citation: Boesten, L.S.M., 2006. Doctoral thesis, Leiden University
ISBN: 908559104X
Sponsor: TNO-Quality of Life, Gaubius Laboratories (afdeling: Vascular and Metabolic Diseases)
Handle: http://hdl.handle.net/1887/4457
 

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