MAPK/ERK signalling is required for zebrafish cardiac regeneration.

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.

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