Myeloid HIF-2⍺ promotes inflammation and worsens cardiac repair after MI. (A) Percent infarct/LV, percent AAR/LV, and percent infarct/AAR measured 3 or 7 d after MI in mice with myeloid-specific deletion of Hif2 (mHIF2^−/−) or controls. n = 5–9 mice/group pooled from more than three independent experiments. *, P < 0.05; **, P < 0.01; ***, P < 0.001 by two-way ANOVA followed by Tukey’s test. (B) Infarct measurement 7 d after MI in mice with overexpression of HIF-2⍺ (mHIF2^LSL) or controls. n = 7 mice/group pooled from two independent experiments. ***, P < 0.001 by two-tailed, unpaired t test. (C) M-mode echocardiography measurements 28 d after MI with quantification of percent ejection fraction (EF), percent fractional shortening (FS), LV systolic and diastolic volume (microliter), LV mass, internal diameter (millimeters), and LV wall thickness (millimeters). n = 9–10 mice/group pooled from two independent experiments. **, P < 0.01, ***, P < 0.001 by two-tailed, unpaired t test. (D) Infarct-associated cellular responses in mHIF2^−/− mice or controls after MI. n = 3–10 mice/group pooled from more than three independent experiments. *, P < 0.05; **, P < 0.01 by two-way ANOVA followed by Tukey’s test. (E) Gene expression of inflammatory mediators in whole cardiac extracts. n = 3–5 mice/group pooled from two independent experiments. *, P < 0.05; **, P < 0.01; ***, P < 0.001 by two-way ANOVA followed by Tukey’s test. (F) OCR of infarct-associated cardiac macrophages 3 d after MI. n = 3–5 mice/group pooled from two independent experiments. *, P < 0.05 by two-tailed, unpaired t test. All data presented as mean ± SEM. D, day.