Scientists have discovered new mechanisms for heart development in mammals

recently, the research results of Zhou Bin Research Group of the Institute of Biochemistry and Cell Biology of the Shanghai Institute of Life Sciences, Chinese Academy of Sciences, were published online on
under the title Identification of a hybrid myocardial zone in the
. The study found new mechanisms of cells and molecules at the center of mammalian heart development.
in the embryonic heart development process, myocardial cell proliferation to the heart cavity protruding mesh heart muscle girder. The small beam of myocardial muscle is responsible for increasing the mass and surface area of myocardial muscle, enhancing the contraction of myocardial muscle, servicing the blood in the chamber and participating in the formation of the heart conduction system. The interwoven mesh heart muscle girder gradually disappeared after the morphological change in the perinatal period. After birth, the heart wall of the heart is mainly composed of dense heart muscle, the inner membrane surface of the heart is relatively smooth. If the morphological change process of myocardial girder is affected, it will lead to incomplete myocardial densification, a congenital cardiomyopathy characterized by excessive girdering of myocardial muscle and thinning of the dense heart muscle layer, with heart failure, arrhythmic disorder and thromboembolism as the main symptoms, due to the main tired left acardial chamber, often referred to as left acardial densification incomplete (LVNC). It is the third most common cardiomyopathy after dilation cardiomyopathy and hypertrophomyopathy. However, the cause of incomplete myocardial edification is not yet clear. It is of great significance to understand the mechanism of lysification of the small beam of the heart muscle of the embryo to clarify the cause of incomplete lying of the left heart chamber. There are two hypothosiss about the mechanism of the transformation of the myocardial girder pattern: one is the hypothesis of dense myocardial layer amplification, which holds that in the late stage of embryonic development or perinatal period, dense myocardial layer amplification fills the gap of mesh heart muscle girder, making the heart muscle small Beams gradually form the heart-tight wall after birth, the other is the myocardial small beam fusion hypothesis, that the heart muscle small beam itself through amplification and fusion to form a post-birth dense chamber wall, and the embryonic dense heart muscle layer does not participate in this process. The difference between the two hypothansures is that the heart muscle beams are transformed into dense chamber walls in different ways.
In order to clarify the mechanism of the denseness of the heart muscle beam, associate researcher Tian Xueying and others, under the guidance of researcher Zhou Bin, used genealogy tracer technology to track the fate of the embryonic myocardial beam and dense heart muscle layer in the heart after birth. The study found that the small beams of the heart muscle in the embryonic stage proliferated less and merged into the endocardial layer of the heart wall; It is composed of heart muscle cells from the heart muscle beam and dense heart muscle layer, and the dense heart muscle layer heart muscle cells multiply into the heart cavity, so that the volume of the heart muscle small beam increases, compresses the small beam gap, and promotes the fusion of the heart muscle beam into the dense heart muscle. In the process of the fusion of the small beams of the heart muscle, the endocardial cells embedded between the small beams are involved in the formation of the endothragm of the coronary artery. This is consistent with the study team's previous findings that the coronary arteries in the inner chamber wall were denser along with the small beams of the heart muscle during the regeneration process.
previous studies have concluded that the inconsemination is not entirely caused by the over-girder of the heart muscle, ignoring the factors that lead to the reduction of the degree of thymthrification caused by the reduction of the involvement of the dense heart muscle layer. The study specifically knocked out the Yap1 gene in the heart muscle cells of the dense myocardial layer during embryonic period, reducing the proliferation of dense myocardial myocardial cells and inhibiting their participation in the formation of the median mixing area of the chamber wall, resulting in excessive girdering of the heart muscle and thinning of the dense heart muscle layer after birth. It is shown that myocardial inconsemination can not be attributed only to the defects of the excess of the heart muscle girder itself, the amplification of the dense myocardial layer during embryonic period and its participation in the formation of the myocardial muscle mixing region are essential for the development of normal myocardial wall, and this study provides important information for further exploration of the pathogenesis of myocardial inconsemination.
research has been supported by the Chinese Academy of Sciences, the Ministry of Science and Technology, the National Natural Science Foundation of China and the Shanghai Science and Technology Commission. (Source: Shanghai Institute of Life Sciences, Chinese Academy of sciences)