Inhibition of p38α MAPK rescues cardiomyopathy induced by overexpressed β₂-adrenergic receptor, but not β₁-adrenergic receptor
J. Clin. Invest. Pallavi S. Peter, et al. 117:1335 doi:10.1172/JCI29576 [Go to this article.]

Figure 1
Echocardiographic measurements of LVEF. Top panels show representative LV M-mode echocardiographic recordings of old WT, old β₂-AR Tg, and old bigenic β₂-AR Tg × DNp38α MAPK mice, showing the dilated, poorly contracting heart in old β₂-AR Tg mice that was rescued in the bigenic β₂-AR Tg × DNp38α MAPK mice. Graphs show mean ± SEM data for LVEF for WT, DNp38α, β₁-AR Tg, β₁-AR Tg × DNp38α MAPK, β₂-AR Tg, and bigenic β₂-AR Tg × DNp38α MAPK mice. The number of mice per group is shown in Table 1. LVEF was significantly increased in young β₁-AR Tg and β₂-AR Tg mice and significantly depressed in old β₁-AR Tg and β₂-AR Tg mice compared with age-matched WT mice. LVEF remained depressed in old bigenic β₁-AR Tg × DNp38α MAPK mice, but in contrast, old bigenic β₂-AR Tg × DNp38α MAPK mice exhibited rescued LV function. *P < 0.05 versus WT; ^†P < 0.05 versus corresponding Tg.