Heng Zhou

TL;DR: Investigation of the potential molecular mechanisms of STING in lipopolysaccharide (LPS)-induced cardiac injury using STING global knockout mice revealed that STING deficiency could alleviate LPS-induced SIC in mice, suggesting that targeting STing in cardiomyocytes may be a promising therapeutic strategy for preventing SIC.

TL;DR: It is concluded that ferritinophagy-mediated ferroptosis is one of the critical mechanisms contributing to sepsis-induced cardiac injury and Targeting ferroPTosis in cardiomyocytes may be a therapeutic strategy for preventing sepsi in the future.

TL;DR: Transgenic mice were resistant to cardiac hypertrophy and fibrosis through inhibition of MEK-ERK1/2 signaling, whereas the Rgs5−/− mice displayed the opposite phenotype in response to pressure overload, indicating that RGS5 protein is a crucial component of the signaling pathway involved in cardiac remodeling and heart failure.

TL;DR: It is shown that IRF8 levels are decreased in human dilated/hypertrophic cardiomyopathic hearts and in murine hypertrophic hearts and thatIRF8 is a potential therapeutic target in pathological cardiac hypertrophy.

TL;DR: The critical roles of miR-133 and its potential mechanisms in cardiac remodeling are summarized and the mechanisms are also sophisticated, involving many target genes and signaling pathways, such as RhoA, MAPK, TGFβ/Smad, and PI3K/Akt.