tetano
Editor, Senior Moderator
Int J Mol Sci
. 2020 Oct 29;21(21):E8081.
doi: 10.3390/ijms21218081.
Emerging Mechanisms of Pulmonary Vasoconstriction in SARS-CoV-2-Induced Acute Respiratory Distress Syndrome (ARDS) and Potential Therapeutic Targets
Harry Karmouty-Quintana[SUP] 1 2 [/SUP], Rajarajan A Thandavarayan[SUP] 3 [/SUP], Steven P Keller[SUP] 4 [/SUP], Sandeep Sahay[SUP] 5 [/SUP], Lavannya M Pandit[SUP] 6 [/SUP], Bindu Akkanti[SUP] 2 [/SUP]
Affiliations
Abstract
The 1918 influenza killed approximately 50 million people in a few short years, and now, the world is facing another pandemic. In December 2019, a novel coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused an international outbreak of a respiratory illness termed coronavirus disease 2019 (COVID-19) and rapidly spread to cause the worst pandemic since 1918. Recent clinical reports highlight an atypical presentation of acute respiratory distress syndrome (ARDS) in COVID-19 patients characterized by severe hypoxemia, an imbalance of the renin-angiotensin system, an increase in thrombogenic processes, and a cytokine release storm. These processes not only exacerbate lung injury but can also promote pulmonary vascular remodeling and vasoconstriction, which are hallmarks of pulmonary hypertension (PH). PH is a complication of ARDS that has received little attention; thus, we hypothesize that PH in COVID-19-induced ARDS represents an important target for disease amelioration. The mechanisms that can promote PH following SARS-CoV-2 infection are described. In this review article, we outline emerging mechanisms of pulmonary vascular dysfunction and outline potential treatment options that have been clinically tested.
Keywords: COVID-19; Kallikrein–Kinin System; acute lung injury; cytokine release storm; endothelin; hypoxic-adenosinergic response; renin angiotensin system; respiratory viral infection.
. 2020 Oct 29;21(21):E8081.
doi: 10.3390/ijms21218081.
Emerging Mechanisms of Pulmonary Vasoconstriction in SARS-CoV-2-Induced Acute Respiratory Distress Syndrome (ARDS) and Potential Therapeutic Targets
Harry Karmouty-Quintana[SUP] 1 2 [/SUP], Rajarajan A Thandavarayan[SUP] 3 [/SUP], Steven P Keller[SUP] 4 [/SUP], Sandeep Sahay[SUP] 5 [/SUP], Lavannya M Pandit[SUP] 6 [/SUP], Bindu Akkanti[SUP] 2 [/SUP]
Affiliations
- PMID: 33138181
- DOI: 10.3390/ijms21218081
Abstract
The 1918 influenza killed approximately 50 million people in a few short years, and now, the world is facing another pandemic. In December 2019, a novel coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has caused an international outbreak of a respiratory illness termed coronavirus disease 2019 (COVID-19) and rapidly spread to cause the worst pandemic since 1918. Recent clinical reports highlight an atypical presentation of acute respiratory distress syndrome (ARDS) in COVID-19 patients characterized by severe hypoxemia, an imbalance of the renin-angiotensin system, an increase in thrombogenic processes, and a cytokine release storm. These processes not only exacerbate lung injury but can also promote pulmonary vascular remodeling and vasoconstriction, which are hallmarks of pulmonary hypertension (PH). PH is a complication of ARDS that has received little attention; thus, we hypothesize that PH in COVID-19-induced ARDS represents an important target for disease amelioration. The mechanisms that can promote PH following SARS-CoV-2 infection are described. In this review article, we outline emerging mechanisms of pulmonary vascular dysfunction and outline potential treatment options that have been clinically tested.
Keywords: COVID-19; Kallikrein–Kinin System; acute lung injury; cytokine release storm; endothelin; hypoxic-adenosinergic response; renin angiotensin system; respiratory viral infection.