Single-cell RNA sequencing reveals Nrg1/ErbB2-induced metabolic reprogramming as a pivotal event for cardiomyocyte proliferation during heart regeneration.
A genome wide transcriptome dataset of the embryonic zebrafish heart with high spatial resolution was established and used to identify a novel mechanism regulating pacemaker function.
The Frank–Starling law of the heart and its underlying mechanism of length-dependent activation involve distinctive structural changes in both the thin and thick filaments of cardiac muscle cells.
Iron derived from autophagy-mediated ferritin degradation in response to pressure overload induces lipid peroxidation, necrotic cardiomyocyte death, and heart failure in mice.
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.
The newly discovered Titin internal promoter may explain why the severity of dilated cardiomyopathy in patients with truncating mutations in Titin varies dramatically depending on position of the mutation.
A precise sequence of left-right asymmetries, combined with mechanical constraints, is sufficient to drive the looped morphogenesis of the embryonic heart tube, with potential impact for congenital heart defects.
Some NKX2-5 mutations that cause congenital heart disease retain transcriptional activity and can bind to many off-target genes, in part through their interactions with cofactors.
Correlative imaging of the heart at multiple spatial scales has the potential to revolutionize the way we understand deficiencies in congenital heart disease.
Heat shock induces relocalization of epigenetic modifiers to the nucleolus, which acts as a dedicated protein quality control center that is indispensable for recovery of epigenetic regulators and epigenetic modifications.
