Cellular Conversations Webinar
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Nov 23
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Paired single-cell multiomics reveals transcriptional circuits governing cell identity and cardiac fibrosis
Cardiac fibrosis is a major driver of heart dysfunction, yet the transcriptional circuits that shape cell identity and push fibroblasts toward a fibrotic state remain poorly understood.
Join Alex Pinto, Head, Cardiac Cellular Systems, Baker Heart and Diabetes Institute as he shares how a paired multiomic approach, capturing both transcriptomic and epigenetic information from the same individual cells, was used to map these circuits in mouse hearts during angiotensin II induced fibrosis and its resolution, as well as in human hearts.
Key insights:
- TF expression or chromatin accessibility alone cannot reliably predict TF activity
- The key regulatory events driving fibrosis are reversible
- A core set of TFs, conserved across mice and humans, regulates the most fibrogenic fibroblasts, including factors not previously linked to cardiac fibrosis
- CREB3L2 modulates extracellular matrix synthesis through distinct nuclear and paracrine mechanisms