MAPK/ERK signalling is required for zebrafish cardiac regeneration
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Updated: Mar 5, 2026
Intrathoracic Injection for the Study of Adult Zebrafish Heart
Published on: May 14, 2019
Peiyun Liu1, Tao P Zhong2,3
1State Key Laboratory of Genetic Engineering, Department of Genetics, Fudan University School of Life Sciences, E203 Life Science Building, 2005 Songhu Road, Shanghai, 200438, China.
Objectives:
To better understand the molecular mechanisms of regeneration and explore the potential signalling pathways as therapeutic targets for heart attacks.
Results:
After treatment with the MEK inhibitor AZD6244 upon cardiac injury, the core members in MAPK/ERK signalling-mek and erk-demonstrate elevated expression, and these proteins are deposited at the injury site in zebrafish. pERK is also induced in non-cardiomyocytes near the injury site. Furthermore, the induced expression of a dominant-negative form of MEK1 inhibits zebrafish cardiac regeneration, characterized by increased cardiac fibrosis (a hallmark of regenerative failure), reduced or delayed production of regenerative myocardium, and migration of FLI1+ endothelial cells, without direct inhibition of cardiomyocyte proliferation.
Conclusion:
Appropriate activation of MAPK/ERK signalling is essential for zebrafish cardiac regeneration.
