deletion is associated with rat embryonic development defects via destruction of KCNH2‑integrin β1 complex.

The Kv11.1 potassium channel encoded by the gene is crucial in conducting the rapid delayed rectifier K current in cardiomyocytes. Homozygous mutation in is embryonically lethal in humans and mice.

Natural Tissue-Imprinted Biointerface for the Topographical Education of a Biomimetic Cell Sheet.

Cell sheet engineering as a cell-based scaffold-free therapy is promising in tissue engineering, allowing precise transforming treatments for various tissue damage. However, the current cutting-edge techniques are still hampered by the difficulty in mimicking the natural tissue organizations and the corresponding physiological functions. In this work, cell-imprinting technology using the natural tissue as a template was proposed to rationally educate the cellular alignment in the cell sheet.

ERG1 plays an essential role in rat cardiomyocyte fate decision by mediating AKT signaling.

ERG1, a potassium ion channel, is essential for cardiac action potential repolarization phase. However, the role of ERG1 for normal development of the heart is poorly understood. Using the rat embryonic stem cells (rESCs) model, we show that ERG1 is crucial in cardiomyocyte lineage commitment via interactions with Integrin β1.

Kcnh2 mediates FAK/AKT-FOXO3A pathway to attenuate sepsis-induced cardiac dysfunction.

Objectives: Myocardial dysfunction is a significant manifestation in sepsis, which results in high mortality. Even Kcnh2 has been hinted to associate with the pathological process, its involved signalling is still elusive.

Materials And Methods: The caecal ligation puncture (CLP) surgery or lipopolysaccharide (LPS) injection was performed to induce septic cardiac dysfunction.

miR-29b-3p protects cardiomyocytes against endotoxin-induced apoptosis and inflammatory response through targeting FOXO3A.

Cardiac dysfunction represents a main component of death induced by sepsis in critical care units. And microRNAs (miRNAs) have been reported as important modulators or biomarkers of sepsis. However, the molecular detail of miRNAs involved in septic cardiac dysfunction remains unclear.