Unfolded Protein Responses in the COVID-19 Context
The endoplasmic reticulum stress response (UPR) maintains cellular homeostasis by regulating key elements of cell growth and defense. Recent evidence suggests that this mechanism influences vascular barrier function by modulating lung endothelial permeability. Dysregulation of this barrier may contribute to the irreversible consequences of acute respiratory distress syndrome (ARDS) caused by SARS-CoV-2. Therefore, targeted activation of these UPR components responsible for repair of the disrupted lung endothelium in COVID-19 patients is likely to offer promising therapeutic possibilities for those exposed to the devastating consequences of the ongoing pandemic.
Nectarios Barabutis
Department of Basic Pharmacy and Toxicology, College of Pharmacy, University of Louisiana at Monroe, 1800 Bienville Drive, Monroe, LA 71201, USA
Received September 4, 2020; revised October 7, 2020; accepted October 8, 2020; available online October 19, 2020.
DESCRIPTION
Lung endothelial barrier dysfunction caused by COVID-19 has been described as a life-threatening problem and a rapid recovery mechanism of endothelial structure contributes to the recovery of respiratory function. This counteracts the SARS-CoV-2-induced cytokine storm-induced hyperpermeability of the lung endothelium, and this study focused on depicting the molecular cascades that regulate the structure and function of the pulmonary microvasculature.
In other words, pharmacological interventions targeting the self-healing endothelium may be useful for COVID-19 treatment. Manipulating the UPR may be of interest because evidence from recent studies indicates that an endothelial regulator called the UPR is involved.Research has described the potential for such measures to be used prophylactically on health care professionals and employees, and future studies on genetically modified mice will describe the exact components involved in these tissue repair processes and the extent of their involvement in the corresponding events.
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