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The study investigates the role of endothelin-converting enzyme-2 (ECE-2) in cardiac development using ECE-2 knockout mice. While ECE-2 null mice are healthy and develop normally, they exhibit more severe cardiac defects when bred with ECE-1 knockout mice, indicating functional redundancy between ECE-1 and ECE-2. The findings suggest that other proteases may also contribute to the activation of endothelins in vivo, highlighting the complexity of cardiac development mechanisms.

Author

minareens

Language

EN