Endothelial Heterogeneity in the Response to Autophagy Drives Small Vessel Muscularization in Pulmonary Hypertension.
Qi ZhangNobuhiro YaoitaArata TabuchiShao-Fei LiuShiau-Haln ChenQiuhua LiNiklas HegemannCaihong LiJulie RodorSara TimmHebatullah LabanToren FinkelTroy StevensDiego F AlvarezLasti ErfinandaMarc de PerrotMariya M KucherenkoChristoph KnosallaMatthias OchsStefanie DimmelerThomas KorffSubodh VermaAndrew H BakerWolfgang M KueblerPublished in: Circulation (2024)
Autophagic activation by hypoxia induces in parallel PAEC proliferation and MVEC apoptosis. These differential responses cause a progressive replacement of MVECs by PAECs in precapillary pulmonary arterioles, thus providing a macrovascular context that in turn promotes pulmonary artery smooth muscle cell proliferation and migration, ultimately driving distal vessel muscularization and the development of PH.
Keyphrases
- pulmonary hypertension
- pulmonary artery
- smooth muscle
- cell death
- single cell
- endoplasmic reticulum stress
- pulmonary arterial hypertension
- cell cycle arrest
- oxidative stress
- endothelial cells
- signaling pathway
- multiple sclerosis
- cell therapy
- fluorescent probe
- minimally invasive
- living cells
- sensitive detection
- stem cells
- mesenchymal stem cells