New Targets That Play A Key Role in Cardiac Repair Were Revealed
Studies in the past two decades have shown that cardiac fibroblasts have plasticity and can be regulated into other types of cells for cardiac repair, such as induced pluripotent stem cells, endothelial cells and cardiomyocytes. Mesenchymal endothelial transformation (MEndoT) has been proved to be beneficial to heart repair, and may represent a new strategy for treating heart disease by transforming cardiac fibroblasts into endothelial phenotype.
Previous studies have shown that MEndoT is partially dependent on P53 signaling pathway; However, there is no in-depth information about the molecular mechanism behind MEndoT. WNT4 plays a key role in the development process and is reactivated in the process of fibrosis injury; However, the role of WNT4 in cardiac repair remains unclear. In this study, the purpose of the researchers is to clarify the pathophysiological role and mechanism of WNT4 in acute myocardial ischemia/reperfusion injury.
Recently, researchers from Guangzhou Medical University published an article entitled "WNT4 is critical for cardiac repair by regulating mesenchymal endothelial transition via the photo JNK/JNK" on the Journal of Theranotics. This research shows that WNT4 plays a key role in heart repair, participates in phosphorylated JNK mediated MEndoT, and is a key gene for cardiac fibroblasts to target treatment of heart disease.
The researchers studied the spatiotemporal expression of WNT4 after acute myocardial ischemia/reperfusion injury, and found that WNT4, as an early injury response gene, was up-regulated in cardiac fibroblasts near the injury boundary, and was related to mesenchymal endothelial transformation (MEndoT), which was a favorable process for blood circulation reconstruction of injured myocardium during cardiac repair.
The researchers proved that WNT4 is a key downstream target gene of P53 in the MEndoT process by chip analysis and in vitro and in vivo function loss and acquisition. Knockout of WNT4 gene in cardiac fibroblasts leads to the decrease of MEndoT and deterioration of cardiac function. In contrast, WNT4 overexpression in cardiac fibroblasts induces MEndoT in these cells through phosphorylated JNK/JNK signaling pathway; However, both P53 and WNT4 protein levels depend on β- Catenin signaling pathway.
JNK activation plays a key role in the induction of MEndoT, and plays a key role in WNT4's regulation of MEndoT. In addition, the specific overexpression of WNT4 in cardiac fibroblasts can save the deterioration of cardiac function caused by P53 gene deletion by reducing fibrosis, increasing MEndoT and vascular density.
In conclusion, the findings of this study indicate that WNT4 has the role of anti fibrosis and promoting endothelial cells in cardiac repair, which not only provides new insights into the mechanism of cardiac repair, but also provides a potential gene for precise regulation of MEndoT in the treatment of heart disease.
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Previous studies have shown that MEndoT is partially dependent on P53 signaling pathway; However, there is no in-depth information about the molecular mechanism behind MEndoT. WNT4 plays a key role in the development process and is reactivated in the process of fibrosis injury; However, the role of WNT4 in cardiac repair remains unclear. In this study, the purpose of the researchers is to clarify the pathophysiological role and mechanism of WNT4 in acute myocardial ischemia/reperfusion injury.
Recently, researchers from Guangzhou Medical University published an article entitled "WNT4 is critical for cardiac repair by regulating mesenchymal endothelial transition via the photo JNK/JNK" on the Journal of Theranotics. This research shows that WNT4 plays a key role in heart repair, participates in phosphorylated JNK mediated MEndoT, and is a key gene for cardiac fibroblasts to target treatment of heart disease.
The researchers studied the spatiotemporal expression of WNT4 after acute myocardial ischemia/reperfusion injury, and found that WNT4, as an early injury response gene, was up-regulated in cardiac fibroblasts near the injury boundary, and was related to mesenchymal endothelial transformation (MEndoT), which was a favorable process for blood circulation reconstruction of injured myocardium during cardiac repair.
The researchers proved that WNT4 is a key downstream target gene of P53 in the MEndoT process by chip analysis and in vitro and in vivo function loss and acquisition. Knockout of WNT4 gene in cardiac fibroblasts leads to the decrease of MEndoT and deterioration of cardiac function. In contrast, WNT4 overexpression in cardiac fibroblasts induces MEndoT in these cells through phosphorylated JNK/JNK signaling pathway; However, both P53 and WNT4 protein levels depend on β- Catenin signaling pathway.
JNK activation plays a key role in the induction of MEndoT, and plays a key role in WNT4's regulation of MEndoT. In addition, the specific overexpression of WNT4 in cardiac fibroblasts can save the deterioration of cardiac function caused by P53 gene deletion by reducing fibrosis, increasing MEndoT and vascular density.
In conclusion, the findings of this study indicate that WNT4 has the role of anti fibrosis and promoting endothelial cells in cardiac repair, which not only provides new insights into the mechanism of cardiac repair, but also provides a potential gene for precise regulation of MEndoT in the treatment of heart disease.
At present, Wuxi Donglin Technology Development Co., Ltd. has developed a variety of Elisa products related to wingless MMTV integration site family member 4. If you want to know about WNT4 Elisa reagent, you can directly visit the website:
http://www.dldevelop.com/research-reagent/dl-wnt4-hu.html
http://www.dldevelop.com/research-reagent/dl-wnt4-mu.html
http://www.dldevelop.com/research-reagent/dl-wnt4-Ra.html
