Zinc Finger Protein ZBTB20 protects against cardiac remodelling post-myocardial infarction via ROS-TNFα/ASK1/JNK pathway regulation.

This study aims to determine the efficacy of Zinc finger protein ZBTB20 in treatment of post-infarction cardiac remodelling. For this purpose, left anterior descending (LAD) ligation was operated on mice to induce myocardial infarction (MI) with sham control group as contrast and adeno-associated virus (AAV9) system was used to deliver ZBTB20 to mouse heart by myocardial injection with vehicle-injected control group as contrast two weeks before MI surgery. Then four weeks after MI, vehicle-treated mice with left ventricular (LV) remodelling underwent deterioration of cardiac function, with symptoms of hypertrophy, interstitial fibrosis, inflammation and apoptosis.

NLRP3 deficiency accelerates pressure overload-induced cardiac remodeling via increased TLR4 expression.

NLRP3, a member of the nucleotide-binding oligomerization domain (NOD)-like receptor family, is involved in cardiac inflammation. However, the functional role of NLRP3 in cardiac remodeling is not clear. To investigate the roles of NLRP3 in pressure overload-induced cardiac remodeling, NLRP3 knockout and wild-type mice were subjected to aortic banding to induce cardiac remodeling.