Abstract
Cardiovascular diseases are a burden on the healthcare and economy of developed countries, because they are among the leading causes of morbidity and mortality. Percutaneous coronary intervention, including stenting, is now an established treatment for coronary artery disease. However, the stent treatment has long been compromised by the limitation of restenosis. The pathology of neointima formation, the fundamental process of vascular restenosis, consists of several sequential steps, i.e., endothelial injury, thrombosis, inflammatory cell adherence to the vessel wall, cytokine and chemokine release, and smooth muscle cell migration and proliferation. To overcome the problem of restenosis, the drug-eluting stent was recently developed. However, this has led to the new concern of late or very late thromboses due to impaired reendothelialization. In this context, the growth factor midkine (MK) shows various interesting characteristics. MK is expressed in the neointima. MK promotes the migration of inflammatory cells as well as smooth muscle cells, and thereby contributes to neointima pathogenesis. MK-deficient mice show reduction in neointima formation. Moreover, MK knockdown can suppress restenosis. Although it remains to be determined whether MK knockdown affects reendothelialization, MK appears to be an attractive molecular target for the next generation of drug-eluting stents.
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I would like to thank all the contributors to the study of MK and vascular restenosis.
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Funding: This work was partly supported by a fund from the Global Center of Excellence Program to Nagoya University from the Ministry of Education, Science, Sport and Culture of Japan.
Conflict of interest: None.
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Kadomatsu, K. (2012). Vascular Restenosis and Midkine. In: Ergüven, M., Muramatsu, T., Bilir, A. (eds) Midkine: From Embryogenesis to Pathogenesis and Therapy. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-4234-5_10
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DOI: https://doi.org/10.1007/978-94-007-4234-5_10
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