Abstract
Right ventricular (RV) remodeling comprises multiple adaptation mechanisms to increased pressure- or volume-overload, which in concert determine RV performance as well as clinical outcome in patients. Here we focus on preclinical models of pressure-overload induced RV remodeling, to better understand a variety of inborn or acquired cardiopulmonary diseases. Analytical tools include genetic, physiologic, and morphologic techniques in animal models ranging from zebrafish to primates. We compare state-of-the-art non-invasive imaging technology with invasive techniques and emphasize the significance of reliable pressure-volume measurements, especially in rodent models. Despite its significant effect on morbidity and mortality, the impact of RV-remodeling under these circumstances was often underestimated. Finally, special attention is given to molecular changes, which reflect recent developments in transciptome and proteome analysis. Unraveling the mechanisms governing transition from the compensated RV to the decompensated status and failure, highlights the importance of translational research in this rapidly evolving field.
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