Key result
Cotreatment with the NPR-C agonist cANF dose-dependently reduced Angiotensin II-induced atrial fibrillation inducibility and prevented atrial fibrosis in wild-type mice.
Why the study?
Mechanisms underlying Ang II-mediated AF are unclear and interventions to prevent its effects are lacking, while cardioprotective natriuretic peptides elicit effects via receptors including NPR-C.
Does NPR-C activation prevent Angiotensin II-induced atrial fibrillation and structural remodeling in mice?
Does NPR-C activation prevent Angiotensin II-induced atrial fibrillation and structural remodeling in mice?
NPR-C activation protects against Angiotensin II-induced atrial fibrillation and structural remodeling in mice, suggesting a potential new therapeutic target.
No takes yet. Share an insight, caveat, or question.
Does not support clinical use of NPR-C agonists for AF; leaves open their potential as a therapeutic target.
Jansen et al. (2019) studied Atrial Fibrillation. NPR-C agonist cANF vs. Angiotensin II alone / NPR-C knockout was evaluated on Atrial fibrillation susceptibility and atrial function. Cotreatment with the NPR-C agonist cANF dose-dependently reduced Angiotensin II-induced atrial fibrillation inducibility and prevented atrial fibrosis in wild-type mice.
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