There is a variety of pathologies and disorders related to left ventricle and ventricular outflow tract that are of a great clinical and scientific importance, for instance congenital heart diseases (ventricular and atrial septal defects, tetrad of Fallot, hypoplastic left heart syndrome), bi-cuspid aortic valve, coarctation of aorta, aortic valve calcification, and non-syndromic dilation of ascending aorta and great vessels.
However, the molecular and genetic mechanisms of these diseases remain largely unknown and need to be clarified. Since left ventricle and ventricular outflow tract derived from the same progenitor cell population, cardiovascular disorders might have common molecular mechanisms implicated in pathogenesis despite clinical differences.
Myocardial stem cells, interstitial cells of the heart valves, and vascular smooth muscle cells are known to play a crucial role in the development of cardiovascular disorders. Impaired signaling results in altered cellular functions, thus underlying myocardial and vascular dysfunction. Currently, attenuations in intracellular signaling pathways developed as a consequence of acquired gene modifications are extensively studied via miscellaneous novel approaches: proteomics, metabolomics, and high-throughput genome screening. These techniques combined with bio-informatics tools allow us to broaden the horizons of our understanding of the fine-tuning of cell functioning.
Here, we propose that recent scientific achievements in the understanding of cell function fine-tuning as well as genetics of left ventricle and ventricular outflow tract disorders would be valuable and make interesting contributions to this Research Topic.
There is a variety of pathologies and disorders related to left ventricle and ventricular outflow tract that are of a great clinical and scientific importance, for instance congenital heart diseases (ventricular and atrial septal defects, tetrad of Fallot, hypoplastic left heart syndrome), bi-cuspid aortic valve, coarctation of aorta, aortic valve calcification, and non-syndromic dilation of ascending aorta and great vessels.
However, the molecular and genetic mechanisms of these diseases remain largely unknown and need to be clarified. Since left ventricle and ventricular outflow tract derived from the same progenitor cell population, cardiovascular disorders might have common molecular mechanisms implicated in pathogenesis despite clinical differences.
Myocardial stem cells, interstitial cells of the heart valves, and vascular smooth muscle cells are known to play a crucial role in the development of cardiovascular disorders. Impaired signaling results in altered cellular functions, thus underlying myocardial and vascular dysfunction. Currently, attenuations in intracellular signaling pathways developed as a consequence of acquired gene modifications are extensively studied via miscellaneous novel approaches: proteomics, metabolomics, and high-throughput genome screening. These techniques combined with bio-informatics tools allow us to broaden the horizons of our understanding of the fine-tuning of cell functioning.
Here, we propose that recent scientific achievements in the understanding of cell function fine-tuning as well as genetics of left ventricle and ventricular outflow tract disorders would be valuable and make interesting contributions to this Research Topic.
