How could perfluorocarbon affect cytokine storm and angiogenesis in coronavirus disease 2019 (COVID-19): role of hypoxia-inducible factor 1α.
Narges MoasefiMehdi FouladiAmir Hossein NorooznezhadReza YaraniAdibeh RahmaniKamaran MansouriPublished in: Inflammation research : official journal of the European Histamine Research Society ... [et al.] (2021)
Coronavirus disease 2019 (COVID-19) pandemic is still a world-class challenge. Inflammation, especially its severe form with excess release of pro-inflammatory cytokines (cytokine storm) which is a life-threatening condition, is among the most important suspects involved in COVID-19 pathogenesis. It has been shown that cytokine storm could cause notable morbidities such as acute respiratory distress syndrome (ARDS) which leads to hypoxia which is significantly associated with mortality of patients with COVID-19. Hypoxia-inducible factor 1α (HIF-1α) which activates following ARDS-induced hypoxia plays a crucial role in pathogenesis of cytokine storm. The expression of tumor necrosis factor α (TNF-α), interleukin 1 β (IL-1β), and IL-6 which are key elements of cytokine storm are by nuclear factor κβ (NFκB). Interestingly, during the hypoxia, HIF-1α activates NFκB to induce expression of pro-angiogenic and pro-inflammatory factors. These released factors starts a autocrine/paracrine loop and causes deterioration of their etiological pathways of expression: cytokine storm and ARDS. To sum up, it seems HIF-1α is an important target to hit to ameliorate the mentioned pathways. Herein, we suggest perfluorocarbons (PFCs) which are among the organofluorine compounds as a possible co-treatment to reduce hypoxemia and then hypoxia. These substances are known for their high gas solving potential that make them able to be used as a synthetic artificial blood product. Due to the potential of PFCs to affect the fountain of important physiopathological pathway such as inflammation a hypoxia through affecting NFκB, they could be considered as multi-target co-treatment for ARD individuals with COVID-19. It is highly suggested to evaluate this hypothesis in following researches.
Keyphrases
- coronavirus disease
- acute respiratory distress syndrome
- endothelial cells
- nuclear factor
- extracorporeal membrane oxygenation
- poor prognosis
- oxidative stress
- mechanical ventilation
- sars cov
- high glucose
- signaling pathway
- respiratory syndrome coronavirus
- rheumatoid arthritis
- toll like receptor
- lps induced
- pi k akt
- long non coding rna
- immune response
- inflammatory response
- vascular endothelial growth factor
- intensive care unit
- cardiovascular events
- diabetic rats
- binding protein
- risk assessment
- human health
- drug induced
- climate change
- replacement therapy
- coronary artery disease