Interplay between cardiac function and heart development

Abstract

Mechanotransduction refers to the conversion of mechanical forces into biochemical or electrical signals that initiate structural and functional remodeling in cells and tissues. The heart is a kinetic organ whose form changes considerably during development and disease. This requires cardiomyocytes to be mechanically durable and able to mount coordinated responses to a variety of environmental signals on different time scales, including cardiac pressure loading and electrical and hemodynamic forces. During physiological growth, myocytes, endocardial and epicardial cells have to adaptively remodel to these mechanical forces. Here we review some of the recent advances in the understanding of how mechanical forces influence cardiac development, with a focus on fluid flow forces. This article is part of a Special Issue entitled: Cardiomyocyte Biology: Integration of Developmental and Environmental Cues in the Heart edited by Marcus Schaub and Hughes Abriel.

A human cell model of cardiac pathophysiological valvulogenesis

“…Valve endothelial cells and their human counterpart iPS cell-derived HPVCs expressing endocardial genes TBX2, TBX20, PITX2, GATA5, SMAD6 and MSX1 (Supplementary Fig. 4), expressed few cilia (data not shown) as recently reported in mouse 46 potentially because the high shear stress in the region of cardiac cushions as proposed in zebrafish 47 . EMT was thus induced by BMP2 treatment of HPVCs and cilia were scored in vimentin+ valvular interstitial cells (Fig.…”

Cardiac remodeling in preterm infants with prolonged exposure to a patent ductus arteriosus

“…During both cardiac development and homoeostatic adaptation, cardiac tissues sense physical forces generated by the heartbeat and respond with changes in gene expression. 29 The role of mechanical forces in shaping the heart during cardiovascular development has been studied in a variety of fetal models, but none are representative for the pressure and volume changes of a PDA. 30 In mice with a surgically placed aortocaval shunt, volume load induces an increase in titin stiffness that can be beneficial and limit eccentric remodeling, but prolonged exposure to volume load leads to further unwanted microscopic changes of the heart.…”

Main Patterns of Fetal Cardiac Remodeling

“…This emphasizes its critical role in distributing blood, nutrients, oxygen, and waste to and from the developing fetus. The heart is a kinetic organ whose structure and form change during development and disease [1]. The prenatal environment will drive the development of the heart so that it has an optimal structure and function given the conditions present.…”