Nuclear factor of activated T-cells 5 is indispensable for a balanced adaptive transcriptional response of lung endothelial cells to hypoxia
Cardiovascular Research2024Vol. 120(13), pp. 1590–1606
Citations Over TimeTop 14% of 2024 papers
Hebatullah Laban, Sophia Siegmund, Katharina Schlereth, Felix A. Trogisch, Alia Ablieh, Lennart Brandenburg, Andreas Weigert, Carolina De La Torre, Carolin Mogler, Markus Hecker, Wolfgang M. Kuebler, Thomas Korff
Abstract
Collectively, our study shows that early and transient subpopulation-specific responses of MLEC to hypoxia may determine the degree of organ dysfunction in later stages. In this context, NFAT5 acts as a protective transcription factor required to rapidly adjust the endothelial transcriptome to cope with hypoxia. Specifically, NFAT5 restricts HIF1α-mediated Pdgfb expression and consequently limits muscularization and resistance of the pulmonary vasculature.
Related Papers
- → miR-29a-3p Attenuates Hypoxic Pulmonary Hypertension by Inhibiting Pulmonary Adventitial Fibroblast Activation(2014)63 cited
- → CSB modulates the competition between HIF-1 and p53 upon hypoxia(2019)18 cited
- → Intermittent short‐duration reoxygenation protects against simulated high altitude‐induced pulmonary hypertension in rats(2020)14 cited
- → Role of Proinfl ammatory Factors, Nitric Oxide, and Some Parameters of Lipid Metabolism in the Development of Immediate Adaptation to Hypoxia and HIF-1α Accumulation(2013)17 cited
- → Reversal of hypoxia by treatment of pulmonary hypertension(2009)