Key result
Angiotensin II injection induces rapid cardiac remodeling in adult zebrafish, marked by hypertrophy and fibrosis.
Why the study?
Understanding pathology upon ectopic activation of hypertension pathways is essential, prompting the development of a zebrafish model to study Angiotensin II-mediated pathogenesis.
This zebrafish model successfully replicates Angiotensin II-induced cardiac pathophysiology seen in mammals, providing a new in vivo platform for studying RAS signaling.
Does not yet inform clinical hypertension management; extends mammalian Ang II remodeling data to a scalable zebrafish platform for RAS studies.
Hypertension, a common chronic condition, may damage multiple organs, including the kidney, heart, and brain. Thus, it is essential to understand the pathology upon ectopic activation of the molecular pathways involved in mammalian hypertension to develop strategies to manage hypertension. Animal models play a crucial role in unraveling the disease pathophysiology by allowing incisive experimental procedures impossible in humans. Zebrafish, a small freshwater fish, have emerged as an important model system to study human diseases. The primary effector, Angiotensin II of the RAS pathway, regulates hemodynamic pressure overload mediated cardiovascular pathogenesis in mammals. There are various established mammalian models available to study pathophysiology in Angiotensin II-induced hypertension. Here, we have developed a zebrafish model to study pathogenesis by Angiotensin II. We find that intradermal Angiotensin II injection every 12 h can induce cardiac remodeling in seven days. We show that Angiotensin II injection in adult zebrafish causes cardiomyocyte hypertrophy and enhances cardiac cell proliferation. In addition, Angiotensin II induces ECM protein-coding gene expression and fibrosis in the cardiac ventricles. Thus, this study can conclude that Angiotensin II injection in zebrafish has similar implications as mammals, and zebrafish can be a model to study pathophysiology associated with AngII-RAS signaling.
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Joshi et al. (2021) studied Angiotensin II-induced cardiac pathophysiology. Angiotensin II vs. PBS (phosphate-buffered saline) was evaluated on Cardiac remodeling (cardiomyocyte hypertrophy, fibrosis, and cell proliferation). Intradermal Angiotensin II injection in adult zebrafish caused cardiac remodeling within 7 days, characterized by cardiomyocyte hypertrophy, fibrosis, and increased cardiac cell proliferation.
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