作者
Q. Zhang,Nobuhiro Yaoita,Arata Tabuchi,Shao‐Fei Liu,Shiau-Haln Chen,Qiuhua Li,Niklas Hegemann,Caihong Li,Julie Rodor,Sara Timm,Hebatullah Laban,Toren Finkel,Troy Stevens,Diego F. Alvarez,Lasti Erfinanda,Marc de Perrot,Mariya M. Kucherenko,Christoph Knosalla,Matthias Ochs,Stefanie Dimmeler,Thomas Korff,Subodh Verma,Andrew H. Baker,Wolfgang M. Kuebler
摘要
Endothelial cell (EC) apoptosis and proliferation of apoptosis-resistant cells is a hallmark of pulmonary hypertension (PH). Yet, why some ECs die and others proliferate and how this contributes to vascular remodeling is unclear. We hypothesized that this differential response may: (1) relate to different EC subsets, namely pulmonary artery (PAECs) versus microvascular ECs (MVECs); (2) be attributable to autophagic activation in both EC subtypes; and (3) cause replacement of MVECs by PAECs with subsequent distal vessel muscularization.