C1QTNF9 and myocardial infarction: Previous research deemed that CTRP9 can activate AMPK after MI, but CTRP9 attenuates adverse post‐MI cardiac remodeling, largely via a PKA‐dependent pathway (Sun et al., 2013); this previous study utilized H9C2 and AMPK‐DN cardiomyocytes and mainly studied apoptosis and fibrosis mechanisms after long‐term MI, whereas in this study, we mainly studied the macrophage polarization process mediated by CTRP9 in the context of early inflammatory transformation post MI.