Here, knockdown of CYP2E1 significantly ameliorated the dilated left ventricle, thin wall, and dysfunctional contraction in the cTnT(R141W) and adriamycin-induced DCM mouse models.
Knockdown or downregulation of CYP2E1 might be a therapeutic strategy to control the development of DCM after mutations of cTnT(R141W) or other factors, because DCM is the third most common cause of heart failure and the most frequent cause of heart transplantation.
Knockdown or downregulation of CYP2E1 might be a therapeutic strategy to control the development of DCM after mutations of cTnT(R141W) or other factors, because DCM is the third most common cause of heart failure and the most frequent cause of heart transplantation.
Knockdown or downregulation of CYP2E1 might be a therapeutic strategy to control the development of DCM after mutations of cTnT(R141W) or other factors, because DCM is the third most common cause of heart failure and the most frequent cause of heart transplantation.