TGFB2 and open-angle glaucoma: Accordingly, silencing of CCN2/CTGF in human ONH astrocytes prevented the increase of ECM proteins following TGF-β2 treatment, leading to the assumption that CCN2/CTGF is an essential factor contributing to the glaucomatous changes in the ONH of POAG patients (Fuchshofer et al., 2005).