scholarly journals Endothelial Hypoxia-Inducible Factor-1α Is Required for Vascular Repair and Resolution of Inflammatory Lung Injury through Forkhead Box Protein M1

2019 ◽  
Vol 189 (8) ◽  
pp. 1664-1679 ◽  
Author(s):  
Xiaojia Huang ◽  
Xianming Zhang ◽  
David X. Zhao ◽  
Jun Yin ◽  
Guochang Hu ◽  
...  
2010 ◽  
Vol 116 (2) ◽  
pp. 673-681 ◽  
Author(s):  
Yogesh Saini ◽  
Krista K. Greenwood ◽  
Christian Merrill ◽  
Kyung Y. Kim ◽  
Sonika Patial ◽  
...  

2017 ◽  
Vol 187 (8) ◽  
pp. 1772-1786 ◽  
Author(s):  
Jazalle McClendon ◽  
Nicole L. Jansing ◽  
Elizabeth F. Redente ◽  
Aneta Gandjeva ◽  
Yoko Ito ◽  
...  

2010 ◽  
Vol 118 (1) ◽  
pp. 318-318
Author(s):  
Ken-ichiro Inoue ◽  
Masako Kiyono ◽  
Yuka Sone ◽  
Hirohisa Takano

Cells ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 183
Author(s):  
Colin E. Evans

Inflammatory lung injury is characterized by lung endothelial cell (LEC) death, alveolar epithelial cell (AEC) death, LEC–LEC junction weakening, and leukocyte infiltration, which together disrupt nutrient and oxygen transport. Subsequently, lung vascular repair is characterized by LEC and AEC regeneration and LEC–LEC junction re-annealing, which restores nutrient and oxygen delivery to the injured tissue. Pulmonary hypoxia is a characteristic feature of several inflammatory lung conditions, including acute lung injury (ALI), acute respiratory distress syndrome (ARDS), and severe coronavirus disease 2019 (COVID-19). The vascular response to hypoxia is controlled primarily by the hypoxia-inducible transcription factors (HIFs) 1 and 2. These transcription factors control the expression of a wide variety of target genes, which in turn mediate key pathophysiological processes including cell survival, differentiation, migration, and proliferation. HIF signaling in pulmonary cell types such as LECs and AECs, as well as infiltrating leukocytes, tightly regulates inflammatory lung injury and repair, in a manner that is dependent upon HIF isoform, cell type, and injury stimulus. The aim of this review is to describe the HIF-dependent regulation of inflammatory lung injury and vascular repair. The review will also discuss potential areas for future study and highlight putative targets for inflammatory lung conditions such as ALI/ARDS and severe COVID-19. In the development of HIF-targeted therapies to reduce inflammatory lung injury and/or enhance pulmonary vascular repair, it will be vital to consider HIF isoform- and cell-specificity, off-target side-effects, and the timing and delivery strategy of the therapeutic intervention.


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