ACTA1 and Right ventricular hypertrophy: Previous studies have proposed that preventing or reversing EndMT typically reduces medial thickening and muscularization, restores endothelial markers (eg, CD31 and VE-cadherin), attenuates mesenchymal/fibrotic markers (eg, α-SMA, vimentin, and collagen I/III), lowers pulmonary pressures, and ameliorates right ventricular hypertrophy.28–30 However, to the best of our knowledge, no selective EndMT inhibitor has been identified, and researchers rely on pleiotropic inhibitors of TGF-β or Wingless-Related Integration Site (Wnt) signaling, anti-inflammatory compounds, or epigenetic modulators.