MAPK3 and Myocardial fibrosis: Besides AHA production, to further clarify whether miR-185 had a potential role in DCM progression through regulating B cells, we detected B cell function in secreting TNF-α, which contributed to low contractility by inducing nitric oxide synthesis, and promoting myocardial fibrosis by facilitating cardiac fibroblasts proliferation and regulating collagen production through ERK1/2 signaling in DCM4, 25, 26.