Abstract
With the term ‘mechanotransduction’, it is intended the ability of cells to sense and respond to mechanical forces by activating intracellular signal transduction pathways and the relative phenotypic adaptation. While a known role of mechanical stimuli has been acknowledged for developmental biology processes and morphogenesis in various organs, the response of cells to mechanical cues is now also emerging as a major pathophysiology determinant. Cells of the cardiovascular system are typically exposed to a variety of mechanical stimuli ranging from compression to strain and flow (shear) stress. In addition, these cells can also translate subtle changes in biophysical characteristics of the surrounding matrix, such as the stiffness, into intracellular activation cascades with consequent evolution toward pro-inflammatory/pro-fibrotic phenotypes. Since cellular mechanotransduction has a potential readout on long-lasting modifications of the chromatin, exposure of the cells to mechanically altered environments may have similar persisting consequences to those of metabolic dysfunctions or chronic inflammation. In the present review, we highlight the roles of mechanical forces on the control of cardiovascular formation during embryogenesis, and in the development and pathogenesis of the cardiovascular system.
Highlights
With the term ‘mechanotransduction’, it is intended the ability of cells to sense and respond to mechanical forces by activating intracellular signal transduction pathways and the relative phenotypic adaptation
Thereafter, the mechanotransduction process continues in adult life, contributing to tissue growth, homeostasis and, disease programming
In adult murine heart, cells with nuclear YAP/TAZ localize at the border zone of the ischemic areas, suggesting a prompt response of resident stromal cells to ischemia in the post infarcted myocardium and a role in collagen deposition and stiffening of myocardial matrix [45]. These findings suggest the existence of a mechanical control of cardiac fibroblast behavior that could be involved in the pathological evolution of cardiac fibrosis disease (Figure 3)
Summary
Stiffness range range (Young’s (Young’s modulus, modulus, kPa) kPa) as as assessed assessed in in aa variety variety of ofhuman humantissues. Cell forces may even contribute to activate genes located in transcription [16] (Figure 1). Cell forces may even contribute to activate genes located in silent heterochromatin domains by promoting access for transcription machinery, re-directing silent heterochromatin domains by promoting access for transcription machinery, re-directing the cell fate towards specific phenotypes [17]. Forces generated by the cytoskeleton are propagated to nuclear lamina to physically stretch the chromatin, and facilitating the binding of the propagated to nuclear lamina to physically stretch the chromatin, and facilitating the binding of the RNA Polymerase II with the transcription factors [18]. Valve and vascular tissues is dependent on their active and passive mechanical properties, and alteration of these characteristics is believed to determine a pathological evolution of tissues
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