COL1A1 and hydrops fetalis: Considering that all the three hub genes—ASPN, COL1A1, and FMOD—are closely associated with the ECM, we thus speculate a potentially key pathway in the development of HF, that is, T-cell-mediated immune responses lead to the imbalance in ECM anabolism and catabolism, ultimately resulting in myocardial fibrosis and HF.