scholarly journals 61 Hypoxia-Inducible Factor 1 (HIF-1) Transcription is a “Signalling Driver” for Allergic Inflammation, Host Innate Immune Defence and Leukaemia Progression

2012 ◽  
Vol 5 ◽  
pp. S20-S21
Author(s):  
Vadim Sumbayev ◽  
Inna Yasinska ◽  
Bernhard Gibbs
2012 ◽  
Vol 446 (1) ◽  
pp. 159-163 ◽  
Author(s):  
Katja Branitzki-Heinemann ◽  
Cheryl Y. Okumura ◽  
Lena Völlger ◽  
Yuko Kawakami ◽  
Toshiaki Kawakami ◽  
...  

MCs (mast cells) are critical components of the host innate immune defence against bacterial pathogens, providing a variety of intra- and extra-cellular antimicrobial functions. In the present study we show, for the first time, that the transcriptional regulator HIF-1α (hypoxia-inducible factor-1α) mediates the extracellular antimicrobial activity of human and murine MCs by increasing the formation of MCETs (MC extracellular traps).


2005 ◽  
Vol 42 (8) ◽  
pp. 903-912 ◽  
Author(s):  
Rachel Dommett ◽  
Matthias Zilbauer ◽  
John T. George ◽  
Mona Bajaj-Elliott

2015 ◽  
Vol 68 (1) ◽  
pp. 40-44 ◽  
Author(s):  
Jos W.M. van der Meer ◽  
Leo A.B. Joosten ◽  
Niels Riksen ◽  
Mihai G. Netea

2014 ◽  
Vol 103 (10) ◽  
pp. 1000-1008 ◽  
Author(s):  
Ylva Kai-Larsen ◽  
Gudmundur H. Gudmundsson ◽  
Birgitta Agerberth

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Elisabetta Ferraro ◽  
Maria Germanò ◽  
Rocco Mollace ◽  
Vincenzo Mollace ◽  
Natalia Malara

Despite the international scientific community’s commitment to improve clinical knowledge about coronavirus disease 2019 (COVID-19), knowledge regarding molecular details remains limited. In this review, we discuss hypoxia’s potential role in the pathogenesis of the maladaptive immune reaction against severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). The state of infection, with serious respiratory dysfunction, causes tissues to become hypoxic due to a discrepancy between cellular O2 uptake and consumption similar to that seen within tumor tissue during the progression of numerous solid cancers. In this context, the heterogeneous clinical behavior and the multiorgan deterioration of COVID-19 are discussed as a function of the upregulated expression of the hypoxia-inducible factor-1 (HIF-1) and of the metabolic reprogramming associated with HIF-1 and with a proinflammatory innate immune response activation, independent of the increase in the viral load of SARS-CoV-2. Possible pharmacological strategies targeting O2 aimed to improve prognosis are suggested.


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