The primary respiratory defect seen in aged cardiomyocytes is an elevated proton leak mediated by ANT1, and this is prevented by treatment with SS-31 (elamipretide).
AKAP6 is a site-specific adaptor required and sufficient to anchor centrosomal proteins and golgi to the nuclear envelope and establishes a non-centrosomal microtubule organization center (ncMTOC).
Brain natriuretic peptide supplementation can increase cardiac neovascularization in infarcted hearts by stimulating endogenous endothelial cell proliferation and proliferation of precursor cells, which will differentiate into endothelial cells.
Macrophage production of MT1-MMP upon MI contributes to adverse cardiac remodeling and worsened function by promoting EndMT via TGFB, suggesting MT1-MMP inhibition as a therapeutic option for patients with MI.
Analyses of human stem cells with distinct GATA6 mutations revealed a spectrum of molecular responses that drive isolated congenital heart disease or the co-occurrence of pancreas and diaphragm malformations.
An integrative structural biology approach provides refined models of the KCNQ1-KCNE1 channel complex, which propose a new mechanism to explain how KCNE1 modulates KCNQ1 channel activation.
Hypoplastic left heart syndrome is reflected by reduced proliferative capacity of patient iPSC-derived cardiomyocytes and requires the activity of LRP2/APOB proteins, likely in conjunction with SHH and WNT signaling pathways.
BIN1 forms a complex with Tau and voltage-gated calcium channels in neurons, and higher BIN1 levels promote neuronal activity, calcium influx, and bursting that is blocked by reducing Tau.
