Inhibition of HIPK2 protects stress-induced pathological cardiac remodeling.

ABSTRACT:

Background

Homeodomain-Interacting Protein Kinase 2 (HIPK2) has been reported to maintain basal cardiac function, however, its role in pathological cardiac remodeling remains unclear.

Methods

HIPK2 inhibitors (tBID and PKI1H) treated mice and two lines of HIPK2^-/- mice were subjected to transverse aortic constriction (TAC). HIPK2 knockdown were performed in neonatal rat cardiomyocytes (NRCMs), neonatal rat cardiac fibroblasts (NRCFs), and human embryonic stem cell-derived cardiomyocytes (hESC-CMs). Microarray analysis was used to screen HIPK2 targets. Overexpression of early growth response 3 (EGR3) and C-type lectin receptor 4D (CLEC4D) were performed in NRCMs, while an activator of Smad3 was used in NRCFs, to rescue the effects of HIPK2 knockdown. Finally, the e

SUBMITTER: Zhou Q 

PROVIDER: S-EPMC9526139 | biostudies-literature | 2022 Nov

REPOSITORIES: biostudies-literature