RNA-sequecning
Congenital heart diseases, characterized by abnormal heart structure, are the most common birth defects around the world. Emerging evidence suggests that mitochondrial homeostasis is required for normal heart development. In mitochondria, a series of molecular chaperones including heat shock protein 60 (HSP60) are engaged in assisting the import and folding of mitochondrial proteins. However, it remains largely obscure whether and how these mitochondrial chaperones regulate cardiac development. Here, we generated a mouse model with cardiac-specific deletion of the Hspd1 gene by aMHC-Cre and investigated the role of HSP60 in embryonic mouse cardiac development. we analyzed the gene expression in both control and HSP60 knockout hearts to figure out the underlysing mechanisms.