IGHE and Myocardial fibrosis: In addition, Zhao et al. found that immunoglobulin E (IgE) and its high-affinity receptor (FcεR1) can promote ventricular remodeling and myocardial fibrosis [90] by suppressing miR-486a-5p, while miR-486-5p could attenuate IgE-FcεR1-induced collagen expression levels and Ang-II-induced cardiac fibrosis.