Myeloid HIF-1⍺ antagonizes cardiac repair through MerTK cleavage 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 Hif1 (mHIF1^−/−) or controls. n = 5–9 mice/group pooled from more than three independent experiments. **, 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-1⍺ (mHIF1^LSL) or controls. n = 6–7 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 (microliters), LV mass, internal diameter (millimeters), and LV wall thickness (millimeters). n = 5–8 mice/group pooled from two independent experiments. **, P < 0.01 by two-tailed, unpaired t test. (D) Infarct-associated cellular responses in mHIF1^−/− mice or controls after MI. n = 4–10 mice/group pooled from more than three independent experiments. **, P < 0.01 by two-way ANOVA followed by Tukey’s test. (E) Phagocytosis of apoptotic mCherry-expressing cardiomyocytes by cardiac macrophages 5 d after MI. n = 4 mice/group pooled from two independent experiments. *, P < 0.05 by two-tailed, unpaired t test. (F) MerTK expression on cardiac macrophages after MI. Unfilled histograms represent FMO staining controls. n = 3–5 mice/group pooled from two independent experiments. *, P < 0.05 by two-way ANOVA followed by Tukey’s test. (G) Serum levels of solMER 3 d after MI. n = 3 mice/group from three independent experiments. **, P < 0.01 by two-tailed, unpaired t test. All data are presented as mean ± SEM.