One limitation of our study is that, although we demonstrate that PFD treatment activates LXR-α and controls the feedback loop of the AT1R/p38-MAPK/RAS axis in a rat model of MI-induced cardiac fibrosis in vivo, further studies should address this issue with gain- or loss-of-function assays in vitro. Here, AGTR1 is linked to myocardial infarction.