Additionally, myeloid-specific PPARγ in a mouse model of MI resulted in increased infarct size, enhanced cardiac hypertrophy, and greater expression of injury markers such as natriuretic peptide b (Bnp) and the oxidative stress enzymes Nox2 and Nox4, revealing a protective mechanism through which macrophage-expressed PPARγ limits the impact of MI [49]. Here, PPARG is linked to myocardial infarction.