自噬
细胞凋亡
医学
肺动脉高压
癌症研究
内皮干细胞
下调和上调
肺动脉
内皮
细胞生物学
心脏病学
免疫学
生物
内科学
体外
基因
生物化学
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
出处
期刊:Circulation
[Lippincott Williams & Wilkins]
日期:2024-06-14
卷期号:150 (6): 466-487
被引量:7
标识
DOI:10.1161/circulationaha.124.068726
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.
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