Human Relaxin-2 Fusion Protein Treatment Prevents and Reverses Isoproterenol-Induced Hypertrophy and Fibrosis in Mouse Heart.

Isoproterenol treatment also showed a trend toward increased phosphorylation of Smad2, a major downstream target of TGFβ1 signaling, as indicated by the increased ratio of phosphorylated Smad2/Smad (Figure 6 H).

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