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. 2017 Nov 21;26:165–174. doi: 10.1016/j.ebiom.2017.11.012

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© 2017 The Authors

This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

PMC Copyright notice

Fig. 2 — Diaph1 deletion reduced myocardial I/R injury. (a) Diaph1 deletion decreased infarct area (% of area at risk) in mouse hearts after LAD/reperfusion vs. WT (n = 10/group; *p < 0.05 vs. WT LAD) while (b) maintaining area at risk. (c) Diaph1 deletion improved fractional shortening after LAD/reperfusion (n = 10/group; *p < 0.05 vs. WT LAD). (d) Diaph1 deletion improved ejection fraction after LAD/reperfusion (n = 10/group; *p < 0.05 vs. WT LAD) (e) Left ventricular developed pressure (LVDP) recovery was improved in hearts isolated from Diaph1^–/– mice compared to WT after ex vivo I/R (n = 6/group; *p < 0.05 vs. WT I/R). (f) LDH release was reduced in shDiaph1 cells after H/R compared to shScr (n = 15–16/group; *p < 0.05 vs. shScr H/R). Unpaired two-tailed t-tests were used; a p-value < 0.05 was considered significant.