Skip to main content
. 2021 May 29;10(12):e019521. doi: 10.1161/JAHA.120.019521

Figure 1. Double deficiency of cyclophilin D and CCR2 showed additive cardioprotection over single deficiency against ischemia‐reperfusion injury.

Figure 1

A‐D, Ratio of infarct size/area at risk in mice subjected to 30, 45, 60, or 90 minutes of myocardial ischemia followed by 24 hours of reperfusion. The horizontal lines represent mean±SD (n=8 per group). *P<0.01, **P < 0.05, 1‐way ANOVA. E, Relationship between the duration of ischemia and infarct size. Redrawn from the data in Figure 1A through 1D. Error bars indicate SD. #1, P<0.0001 vs 30 minutes, #2; P<0.0001 vs 30 minutes, P<0.05 vs 45 minutes; #3, P<0.0001 vs 30 minutes, P<0.001 vs 45 minutes; #4 P<0.01 vs 30 minutes; #5, P<0.0001 vs 30 minutes, P<0.0001 vs 45 minutes; #6, P<0.0001 vs 30 minutes, P<0.0001 vs 45 minutes, P<0.001 vs 60 minutes; #7, P<0.01 vs 30 minutes; #8, P<0.0001 vs 30 minutes; #9, P<0.0001 vs 30 minutes, P<0.001 vs 45 minutes, P<0.01 vs 60 minutes; #10, P<0.0001 vs 30 minutes, P<0.0001 vs 45 minutes; #11, P<0.0001 vs 30 minutes, P<0.0001 vs 45 minutes, P<0.001 vs 60 minutes, 2‐way ANOVA. CCR2‐KO indicates C‐C chemokine receptor 2‐knockout mice; CypD‐KO, cyclophilin D‐knockout mice; Double‐KO, cyclophilin‐D/C‐C chemokine receptor 2‐double knockout mice; mPTP, mitochondrial permeability transition pore; and WT indicates wild‐type mice.