Key result
Loss of Zfpm1 activity in zebrafish resulted in compromised cardiac function, deformed trabecular meshwork, over-activation of Neuregulin-ErbB signalling, and elevated cardiomyocyte proliferation.
Why the study?
How early trabeculae carneae forms and subsequently develops into mature chambers is poorly understood.
Does loss of Zfpm1 activity affect ventricular trabeculation and cardiac function in zebrafish?
Does loss of Zfpm1 activity affect ventricular trabeculation and cardiac function in zebrafish?
The zinc finger protein Zfpm1 plays a pivotal role in coordinating ventricular trabeculae patterning and growth through modulation of Neuregulin-ErbB signalling.
Answers are grounded in this paper and cite their sources.
No immediate clinical implications; leaves open Zfpm1's role in mammalian trabeculation and function.
Ventricular trabeculation is one essential step for generating a functionally competent ventricular wall, while how the early trabeculae carneae forms and subsequently develops into mature chambers is poorly understood. We found that in zebrafish zfpm1-/- juvenile, cardiac function is significantly compromised, with hearts exhibiting deformed trabecular meshwork. To elucidate the mechanisms of Zfpm1 function in cardiac trabeculation, we analyzed zfpm1 mutant hearts more closely and found that loss of Zfpm1 activity resulted in over-activation of Neuregulin-ErbB signalling and abnormally elevated cardiomyocyte proliferation during cardiac trabeculae growth and modeling stages. These results implicate Zfpm1 plays a pivotal role in coordinating trabeculae patterning and growth.
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Yang et al. (2019) studied Ventricular trabeculation and cardiac function. Loss of Zfpm1 activity (zfpm1-/- mutation) vs. Wild-type (implied) was evaluated on Cardiac function, trabecular meshwork formation, Neuregulin-ErbB signalling, and cardiomyocyte proliferation. Loss of Zfpm1 activity in zebrafish resulted in compromised cardiac function, deformed trabecular meshwork, over-activation of Neuregulin-ErbB signalling, and elevated cardiomyocyte proliferation.
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