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Enhancing mitochondrial Ca²⁺ uptake effectively suppresses aberrant Ca²⁺ induced arrhythmogenic events in zebrafish, mouse and human cardiomyocytes, demonstrating a critical role for mitochondria in the regulation of cardiac rhythmicity.

Mapping the locations of hypertrophic cardiomyopathy gene variants onto the three-dimensional structures of contractile proteins revealed that these disrupt protein interactions are critical for normal cardiac relaxation and efficient energy usage.

Starfish feed by everting their stomach out of their mouth over prey and, interestingly, this unusual feeding mechanism is inhibited by substances similar to hormones that regulate feeding in humans.

Ablation of the sarcomeric protein myopalladin (MYPN), associated with human cardiomyopathies, results in dilated cardiomyopathy, which is severely aggravated by biomechanical stress, suggesting that skeletal myopathy patients carrying MYPN loss-of-function mutations may develop cardiomyopathy under conditions of cardiac stress.

The combination of high-speed light sheet microscopy and suitable data analysis facilitates cell-accurate measurements across entire organs and opens the way to systematic, scale-bridging, in vivo studies of organogenesis.

Calcium overload in cardiomyocytes disrupts sarcomere integrity, by stimulating transcriptional upregulation of the E3 ubiquitin ligase MuRF1.

Cardiac fibroblast reduction is well-tolerated and demonstrates beneficial outcomes after heart injury.

Correlative imaging of the heart at multiple spatial scales has the potential to revolutionize the way we understand deficiencies in congenital heart disease.

The transcription factor Snai1b maintains the myocardial wall integrity by limiting cell extrusions and regulating the intermediate filament gene desmin b.