Abstract.
Numerous studies in animal models established a key role of the C-jun N-terminal kinase (JNK) family (JNK1, JNK2 and JNK3) in numerous pathological conditions, including cancer, cardiac hypertrophy and failure, neurodegenerative disorders, diabetes, arthritis and asthma. A possible function of JNK in atherosclerosis remained uncertain since conclusions have mainly been based on in vitro studies investigating endothelial cell activation, T-effector cell differentiation and proliferation of vascular smooth muscle cells, all of which represent crucial cellular processes involved in atherosclerosis. However, recent experiments demonstrated that macrophage-restricted deletion of JNK2 was sufficient to efficiently reduce atherosclerosis in mice. Furthermore, it has been shown that JNK2 specifically promotes scavenger receptor A-mediated foam cell formation, an essential step during early atherogenesis, which occurs when vascular macrophages internalize modified lipoproteins. Thus, specific inhibition of JNK2 activity may emerge as a novel and promising therapeutic approach to attenuate atheroma formation in the future. In this review, we discuss JNK-dependent cellular and molecular mechanisms underlying atherosclerosis.
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Received 9 June 2005; received after revision 18 July 2005; accepted 18 July 2005
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Sumara, G., Belwal, M. & Ricci, R. “Jnking” atherosclerosis. Cell. Mol. Life Sci. 62, 2487–2494 (2005). https://doi.org/10.1007/s00018-005-5253-6
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DOI: https://doi.org/10.1007/s00018-005-5253-6