Figure 4. G_αq as a critical target of RGS2.

(A) Inhibition of PLCβ with U73122 prevents exacerbated hypertrophy (heart weight/tibia length), chamber dilation, and dysfunction (n = 7–14 per group). *P < 0.001 versus other groups. (B) In Rgs2^–/– mice subjected to 48 h TAC, the inactive control agent U73343 did not suppress pathological remodeling. Summary echo data are provided in Supplemental Figure 2B. (C) Cardiac hypertrophy was exacerbated in double-mutant G_αq-OE⁺Rgs2^–/– mice (n = 7–9 per group). **P < 0.01 versus other groups. (D) Corresponding echocardiograms showed worsened function and chamber dilation. (E) Summary data for LV diastolic dimension, FS, and heart rate (n = 7–9 per group). *P < 0.05 versus other groups; ^†P < 0.05 versus all G_αq-OE^– groups. (F) Response of cardiac LV mass and echocardiographic FS in mice subjected to swimming versus sedentary animals. Exercise-induced hypertrophy was similar in Rgs2^+/+ and Rgs2^–/– mice, with no change in FS. *P < 0.01, ^†P < 0.05 versus respective week-0 baseline.