scholarly journals Hypoxia‐Inducible Factor (HIF)‐1α induced regulation of lung injury in pulmonary aspiration is mediated through NF‐kB

2021 ◽  
Author(s):  
Suresh V Madathilparambil ◽  
George Yalamanchili ◽  
Tejeshwar C. Rao ◽  
Sinan Aktay ◽  
Alex Kralovich ◽  
...  
Keyword(s):  
Lung Injury ◽  
Hypoxia Inducible Factor ◽  
Pulmonary Aspiration

scholarly journals Inhibition of hypoxia inducible factor-1α ameliorates lung injury induced by trauma and hemorrhagic shock in rats

2012 ◽  
Vol 33 (5) ◽  
pp. 635-643 ◽  
Author(s):  
Hong Jiang ◽  
Yan Huang ◽  
Hui Xu ◽  
Rong Hu ◽  
Qi-fang Li
Keyword(s):  
Lung Injury ◽  
Hemorrhagic Shock ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1Α

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 ◽  
...  
Keyword(s):  
Lung Injury ◽  
Hypoxia Inducible Factor ◽  
Vascular Repair ◽  
Hypoxia Inducible Factor 1Α ◽  
Forkhead Box

Hypoxia-inducible factor prolyl-hydroxylase inhibitor roxadustat (FG-4592) alleviates sepsis-induced acute lung injury

2020 ◽  
Vol 281 ◽  
pp. 103506
Author(s):  
Fu Han ◽  
Gaofeng Wu ◽  
Shichao Han ◽  
Zhenzhen Li ◽  
Yanhui Jia ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Hypoxia Inducible Factor ◽  
Prolyl Hydroxylase ◽  
Prolyl Hydroxylase Inhibitor

scholarly journals Acute Cobalt-Induced Lung Injury and the Role of Hypoxia-Inducible Factor 1α in Modulating Inflammation

2010 ◽  
Vol 116 (2) ◽  
pp. 673-681 ◽  
Author(s):  
Yogesh Saini ◽  
Krista K. Greenwood ◽  
Christian Merrill ◽  
Kyung Y. Kim ◽  
Sonika Patial ◽  
...  
Keyword(s):  
Lung Injury ◽  
Hypoxia Inducible Factor ◽  
Hypoxia Inducible Factor 1Α

scholarly journals Hypoxia-Inducible Factor (HIF)-1α Promotes Inflammation and Injury Following Aspiration-Induced Lung Injury in Mice

Shock ◽  
2019 ◽  
Vol 52 (6) ◽  
pp. 612-621 ◽  
Author(s):  
Madathilparambil V. Suresh ◽  
Sanjay Balijepalli ◽  
Boya Zhang ◽  
Vikas Vikram Singh ◽  
Samantha Swamy ◽  
...  
Keyword(s):  
Lung Injury ◽  
Hypoxia Inducible Factor

scholarly journals Hypoxia-Inducible Factor 1α Signaling Promotes Repair of the Alveolar Epithelium after Acute Lung Injury

2017 ◽  
Vol 187 (8) ◽  
pp. 1772-1786 ◽  
Author(s):  
Jazalle McClendon ◽  
Nicole L. Jansing ◽  
Elizabeth F. Redente ◽  
Aneta Gandjeva ◽  
Yoko Ito ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Hypoxia Inducible Factor ◽  
Alveolar Epithelium ◽  
Hypoxia Inducible Factor 1Α

Abstract 12651: Fine-Tuning of Lung Thrombosis is a Therapeutic Strategy Against Inflammatory Lung Injury

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Colin E Evans ◽  
Xianming Zhang ◽  
Narsa Machireddy ◽  
You-yang Zhao
Keyword(s):  
Lung Injury ◽  
Therapeutic Strategy ◽  
Hypoxia Inducible Factor ◽  
Fine Tuning ◽  
Dependent Manner ◽  
Murine Models ◽  
Survival Gene ◽  
The Impact ◽  
Dose Dependent ◽  
Different Levels

Introduction: Lung thrombosis (LT) and endothelial cell (EC) death are positively associated with mortality in sepsis-induced acute lung injury (ALI) patients, but anti-coagulants have failed in clinical trials of sepsis. Hypothesis: We hypothesized that different levels of LT mediate ALI by regulating lung EC viability. Methods: To assess the impact of different levels of LT on ALI, we used murine models of LT and ALI. To explore how LT level might alter lung EC viability and ALI, we assessed survival gene expression by RNA sequencing. To identify the mechanism(s) responsible for changes in ALI after varying levels of LT, we assessed lung EC viability and ALI in mice with cell-specific knockout of different survival genes. Results: In platelet-depleted mice, LT was reduced while ALI was increased. Intra-venous microbeads were then administered to induce LT in a dose-dependent manner, showing that restoration of LT to the level found in platelet-replete mice protected against thrombocytopenia-induced ALI. We next showed in wild type mice, that while excessive increases in LT worsened ALI, induction of a mild level of LT conversely protected against ALI. The opposing impact of diminished or excessive versus mild LT on ALI was associated with changes in lung EC apoptosis. Subsequent studies showed a panel of candidate survival factors were differentially expressed in the lungs of ALI mice with or without mild or excessive LT. Mechanistically, we found that the protective impact of mild LT on ALI is dependent upon hypoxia-inducible factor (HIF) 1α in Tie2-expressing cells. Remarkably, the same mild level of LT retained its protective impact in platelet-depleted and platelet-replete mice even when induced up to 8 hours after sepsis. Conclusions: ALI is enhanced by diminished or excessive LT but suppressed by mild LT through HIF1α. The control of LT represents a therapeutic strategy for the induction of a pro-survival response that protects against inflammatory lung injury.

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