Key result
Beta-3 adrenergic receptor activation drives cardiac fibroblast fibrosis via biased beta-arrestin2 signaling.
Demonstrates that beta3-adrenergic receptor activation drives fibrosis in cardiac fibroblasts via beta-arrestin2, suggesting a path toward cell-specific heart failure therapeutics.
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Ali Hussein Eid (2026) conducted an editorial in Heart failure. β3-adrenergic receptor activation was evaluated. β3-adrenergic receptor activation promotes a profibrotic phenotype in cardiac fibroblasts through β-arrestin2-mediated biased signalling, independently of classical Gi protein coupling.
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