Juan Manuel González‐Rosa

This study shows that overexpression of TNNI3K in zebrafish impairs heart regeneration by causing chronic inflammation and fibrosis rather than cell-cycle defects.

This paper describes a cryoinjury model in zebrafish to study liver regeneration by inducing localized necrosis, inflammation, and fibrosis.

The paper optimizes methods to generate cardiomyocyte-specific CRISPR mutants in zebrafish using the cardiodeleter system, enabling rapid and robust gene deletion with detailed protocols.

This paper develops a hepatic cryoinjury model to study liver regeneration and fibrosis, showing it enables comparison of healthy and injured tissue in the same animal.

The paper identifies actomyosin dynamics and Notch/Bmp signaling as drivers of apical extrusion of proepicardial cells in zebrafish during heart development.

The paper investigates fibrosis resolution in regenerating zebrafish hearts, finding that fibroblasts become inactivated rather than being eliminated, and that fibrosis supports cardiomyocyte proliferation.