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Journal Article

Molecular etiology of atherogenesis--in vitro induction of lipidosis in macrophages with a new LDL model

MPS-Authors
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Sampaio,  Julio
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

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Shevchenko,  Andrej
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

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Verkade,  Paul
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

Vaz,  Winchil
Max Planck Society;

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Vieira,  Otilia V
Max Planck Institute of Molecular Cell Biology and Genetics, Max Planck Society;

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Citation

Estronca, L. M. B. B., Silva, J. S. D., Sampaio, J., Shevchenko, A., Verkade, P., Vaz, A. D. N., et al. (2012). Molecular etiology of atherogenesis--in vitro induction of lipidosis in macrophages with a new LDL model. PLoS ONE, 7(4): e34822.


Cite as: https://hdl.handle.net/21.11116/0000-0001-0866-4
Abstract
Atherosclerosis starts by lipid accumulation in the arterial intima and progresses into a chronic vascular inflammatory disease. A major atherogenic process is the formation of lipid-loaded macrophages in which a breakdown of the endolysomal pathway results in irreversible accumulation of cargo in the late endocytic compartments with a phenotype similar to several forms of lipidosis. Macrophages exposed to oxidized LDL exihibit this phenomenon in vitro and manifest an impaired degradation of internalized lipids and enhanced inflammatory stimulation. Identification of the specific chemical component(s) causing this phenotype has been elusive because of the chemical complexity of oxidized LDL.