**1. Introduction**

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122 Calcific Aortic Valve Disease

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> With a growing older population, cardiovascular diseases are becoming an increasing economic and social burden in Western societies. Cardiovascular calcification is a major characteristic of chronic inflammatory disorders — such as chronic renal disease (CRD), type 2 diabetes (T2D), atherosclerosis and calcific aortic valve disease (CAVD) — that associate with significant morbidity and mortality. Cardiovascular calcification also associates with osteoporosis in humans and animal models [1, 2] — the so-called "calcifica‐ tion paradox" [3]. The concept that similar pathways control both bone remodeling and vascular calcification is currently widely accepted, but the precise mechanisms of calcifica‐ tion remain largely unknown. Osteogenic transition of vascular smooth muscle cells (SMCs), valvular interstitial cells (VIC) or stem cells is induced by bone morphogenetic proteins, inflammation, oxidative stress, or high phosphate levels, and leads to a unique molecular pattern marked by osteogenic transcription factors [4]. Loss of mineralization inhibitors, such as matrix γ-carboxyglutamic acid Gla protein (MGP) and fetuin-A also contribute to cardiovascular calcification. The physiological balance between induction and inhibition of calcification becomes dysregulated in CRD, T2D, atherosclerosis, and CAVD. Consequently, calcification may occur at several sites in the cardiovascular system, including the intima and media of vessels and cardiac valves [3].

> The central role of miRNAs as fine-tune regulators in the cardiovascular system and bone biology has gained acceptance and has raised the possibility for novel therapeutic targets. Circulating miRNAs have been proposed as biomarkers for a wide range of cardiovascu‐ lar diseases, but knowledge of miRNA biology in cardiovascular calcification is very limited.

© 2013 Goettsch and Aikawa; licensee InTech. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. © 2013 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
