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These show that neuregulin-1 induces cardiomyocyte Feret elongation via sustained PI3K signaling, while transient p38 signaling increases cell size but not shape. This study leverages experimental-computational methods to dissect how signaling dynamics distinctly regulate cell size vs. shape. 3/3

We first characterized the proteomic, gene expression, and phenotypic responses of cardiomyocytes (including our new cell shape metric Feret elongation) to diverse ligands. We integrated this data with data-driven and mechanistic computational models, validated with new perturbation experiments. 2/

I would say that tracks but...

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Finally, check out the eye candy! Awesome multi-channel live-cell videos analyzed with machine learning segmentation and tracking. Shows the complex fates that cells commit to. 3/3

Inhibition of caspase-3 changes a cell's bias from apoptosis to hypertrophy. Initial cell and nuclear morphological features also bias a cell's decisions. These results demonstrate that the single-cell dynamics of cardiomyocyte growth and death are highly heterogeneous and dynamic. 2/3

Thanks! The Point, Rose River Loop, Big Meadows

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Further, pharmacologic and postnatal genetic inhibition of DYRK1A enhanced cardiomyocyte cycling and cardiac functional recovery after MI. Overall, our findings reveal network mechanisms by which a small molecule inhibitor drives cardiomyocyte cycling and post-MI functional recovery. 3/3

We used network modeling to predict mechanisms by which DYRK1A inhibition induces cardiomyocyte cell cycling. We validated these predictions using a recently described small molecular inhibitor of DYRK1A by imaging and RNA sequencing of cultured cardiomyocytes. 2/3

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