Fig. 10: Working model and summary of our study. | Nature Communications

Fig. 10: Working model and summary of our study.

From: Border-zone cardiomyocytes and macrophages regulate extracellular matrix remodeling to promote cardiomyocyte protrusion during cardiac regeneration

Fig. 10

A Working model of CM invasion to replace injured tissue during zebrafish heart regeneration. CM-intrinsic mechanisms, partly regulated by AP-1 transcription factors, promote actin cytoskeletal remodeling/organization and protrusion formation, while Mmp14b and macrophages contribute to remodeling the ECM at the border zone to create a permissive environment for CM invasion. Created in BioRender. Beisaw, A. (2025) https://BioRender.com/19dzxy0. B Summary of the genetic models presented in our study and their effects on CM protrusion and invasion, including CM:A-Fos to block AP-1, mmp14b deletion, CM:mmp14b OE, and CM:mmp14b OE in the absence of macrophages. The effects of mmp14b deletion on endothelial cells (blood vessels) in the model is from previously published data68. BZ border zone, CM cardiomyocyte, ECM extracellular matrix, Fb fibroblast, mϕ macrophage, OE overexpression.

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