Abstract
Collagen fibers are essential structural components of mitral valve leaflets, their tension apparatus (chordae tendineae), and the associated papillary muscles. Excess or lack of collagen fibers in the extracellular matrix (ECM) in any of these structures can adversely affect mitral valve function. The organization of collagen fibers provides a sophisticated framework that allows for unidirectional blood flow during the precise opening and closing of this vital heart valve. Although numerous ECM molecules are essential for the differentiation, growth, and homeostasis of the mitral valve (e.g., elastic fibers, glycoproteins, and glycans), collagen fibers are key to mitral valve integrity. Besides the inert structural components of the tissues, collagen fibers are dynamic structures that drive outside-to-inside cell signaling, which informs valvular interstitial cells (VICs) present within the tissue environment. Diversity of collagen family members and the closely related collagen-like triple helix-containing proteins found in the mitral valve, will be discussed in addition to how defects in these proteins may lead to valve disease.
Highlights
The mechanical integrity of the mitral valve largely depends on its extracellular matrix (ECM) composition, as the cells provide only little to no mechanical strength [1]
While the elastic fibers play an essential role in mitral valve function, it is the collagen fibers with the proper tensile strength to maintain tissue integrity during peak systole (~120 mmHg blood pressure applied over the surface of the human mitral valve)
They work in concert with the collagen fibers in valve tissue throughout the cardiac cycle, in chordae tendineae where they are thought to be essential for the molecular crimping and uncrimping of these fibers as they are loaded and unloaded during systole and diastole [2]
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. As the valve tissues mature, the cells of the chordae begin to express increasing amounts of periostin and fibril-forming collagens such as type I [10]. In the mitral valve of larger vertebrates, crimped collagen fibers are found in all the chordae and throughout the collagen dense regions of the leaflets, though in different periodicities [2]. It appears that this crimped collagen fiber conformation forms relatively late (perinatal) during the heart development and is presaged by type VI collagen expression. In the left ventricle affect mitral valve cell viability and ECM maintenance
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