Acute Respiratory Distress Syndrome and COVID-19: A Literature Review

Hussain, Musaddique; Syed, Shahzada Khurram; Fatima, Mobeen; Shaukat, Saira; Saadullah, Malik; Alqahtani, Ali; Alqahtani, Taha; Emran, Talha Bin; Alamri, Ali H.; Barkat, Muhammad Qasim; Wu, Ximei

doi:10.2147/jir.s334043

Cited by 25 publications

(16 citation statements)

References 131 publications

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“…According to the American-European Consensus Conference on acute respiratory distress syndrome (ARDS), the ARDS is the most severe form of the acute lung injury [ 17 ] as well as ongoing COVID-19 associated lethality [ 18 ]. Pulmonary capillary endothelium provides a fertile “soil” for viral entry, replication, thereby facilitating viral entry to the circulating blood [ 19 , 20 ].…”

Section: Endothelial Dysfunction and Covid-19 Associated Multi-organ ...mentioning

confidence: 99%

Endothelial dysfunction in COVID-19: an overview of evidence, biomarkers, mechanisms and potential therapies

2022

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The fight against coronavirus disease 2019 (COVID-19) caused by SARS-CoV-2 infection is still raging. However, the pathophysiology of acute and post-acute manifestations of COVID-19 (long COVID-19) is understudied. Endothelial cells are sentinels lining the innermost layer of blood vessel that gatekeep micro- and macro-vascular health by sensing pathogen/danger signals and secreting vasoactive molecules. SARS-CoV-2 infection primarily affects the pulmonary system, but accumulating evidence suggests that it also affects the pan-vasculature in the extrapulmonary systems by directly (via virus infection) or indirectly (via cytokine storm), causing endothelial dysfunction (endotheliitis, endothelialitis and endotheliopathy) and multi-organ injury. Mounting evidence suggests that SARS-CoV-2 infection leads to multiple instances of endothelial dysfunction, including reduced nitric oxide (NO) bioavailability, oxidative stress, endothelial injury, glycocalyx/barrier disruption, hyperpermeability, inflammation/leukocyte adhesion, senescence, endothelial-to-mesenchymal transition (EndoMT), hypercoagulability, thrombosis and many others. Thus, COVID-19 is deemed as a (micro)vascular and endothelial disease. Of translational relevance, several candidate drugs which are endothelial protective have been shown to improve clinical manifestations of COVID-19 patients. The purpose of this review is to provide a latest summary of biomarkers associated with endothelial cell activation in COVID-19 and offer mechanistic insights into the molecular basis of endothelial activation/dysfunction in macro- and micro-vasculature of COVID-19 patients. We envisage further development of cellular models and suitable animal models mimicking endothelial dysfunction aspect of COVID-19 being able to accelerate the discovery of new drugs targeting endothelial dysfunction in pan-vasculature from COVID-19 patients.

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Section: Endothelial Dysfunction and Covid-19 Associated Multi-organ ...mentioning

confidence: 99%

Endothelial dysfunction in COVID-19: an overview of evidence, biomarkers, mechanisms and potential therapies

2022

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“… 169 , 170 It is worth mentioning that corticosteroids may present different outcomes in ARDS subjects depending on several factors, including the timing of initiation of treatment, the origin of ARDS, type and dose of corticosteroid, and among others (for a review on corticosteroids and ARDS, see Hussain et al . 171 ).…”

Section: Drugs Used To Reduce the Coronaviruses-induced Enhanced Perm...mentioning

confidence: 99%

Effect of coronaviruses on blood vessel permeability: potential therapeutic targets

Machado

Dias

Cortes

et al. 2023

Ther Adv Respir Dis

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Coronavirus-induced diseases have afflicted humanity for several decades. This scenario was aggravated by the emergence of the coronavirus disease 2019 (named COVID-19) in Wuhan, China, in December 2019. Since then, COVID-19 has killed millions of people worldwide, probably the most devastating pandemic since HIV/AIDS. This review aimed to bring together important updated aspects related to coronavirus-induced diseases and the enhanced vascular permeability observed mainly in the lungs of affected people. The dysregulated vascular permeability in the lungs is of fundamental importance for coronaviruses-caused morbidity and mortality. Thus, as described in this review, it is a target of new and old drugs.

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“…Most notably, the lungs are a highly vulnerable organ wherein pulmonary inflammation and infection result in vascular leakage and thereby the development of ARDS 5,6 . Indeed, many patients with severe coronavirus disease 2019 (COVID‐19), a newly emerging infectious disease of major concern, have developed ARDS, the main cause of mortality in those affected 7 …”

Section: Introductionmentioning

confidence: 99%

“…5,6 Indeed, many patients with severe coronavirus disease 2019 (COVID- 19), a newly emerging infectious disease of major concern, have developed ARDS, the main cause of mortality in those affected. 7 Vascular endothelial (VE)-cadherin is an EC-specific cell adhesion molecule involved in the formation of adherens junctions (AJs) that regulate vascular permeability mainly in peripheral tissues. VE-cadherin-based AJs exist in two forms; stable linear AJs supported by circumferential actin bundles (CABs) and focal AJs connected by radial stress fibers (RSF).…”

Section: Introductionmentioning

confidence: 99%

Rap1 small GTPase is essential for maintaining pulmonary endothelial barrier function in mice

Yamamoto,

Watanabe‐Takano,

Oguri‐Nakamura

et al. 2023

The FASEB Journal

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Vascular permeability is dynamically but tightly controlled by vascular endothelial (VE)‐cadherin‐mediated endothelial cell–cell junctions to maintain homeostasis. Thus, impairments of VE‐cadherin‐mediated cell adhesions lead to hyperpermeability, promoting the development and progression of various disease processes. Notably, the lungs are a highly vulnerable organ wherein pulmonary inflammation and infection result in vascular leakage. Herein, we showed that Rap1, a small GTPase, plays an essential role for maintaining pulmonary endothelial barrier function in mice. Endothelial cell‐specific Rap1a/Rap1b double knockout mice exhibited severe pulmonary edema. They also showed vascular leakage in the hearts, but not in the brains. En face analyses of the pulmonary arteries and 3D‐immunofluorescence analyses of the lungs revealed that Rap1 potentiates VE‐cadherin‐mediated endothelial cell–cell junctions through dynamic actin cytoskeleton reorganization. Rap1 inhibits formation of cytoplasmic actin bundles perpendicularly binding VE‐cadherin adhesions through inhibition of a Rho‐ROCK pathway‐induced activation of cytoplasmic nonmuscle myosin II (NM‐II). Simultaneously, Rap1 induces junctional NM‐II activation to create circumferential actin bundles, which anchor and stabilize VE‐cadherin at cell–cell junctions. We also showed that the mice carrying only one allele of either Rap1a or Rap1b out of the two Rap1 genes are more vulnerable to lipopolysaccharide (LPS)‐induced pulmonary vascular leakage than wild‐type mice, while activation of Rap1 by administration of 007, an activator for Epac, attenuates LPS‐induced increase in pulmonary endothelial permeability in wild‐type mice. Thus, we demonstrate that Rap1 plays an essential role for maintaining pulmonary endothelial barrier functions under physiological conditions and provides protection against inflammation‐induced pulmonary vascular leakage.

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Acute Respiratory Distress Syndrome and COVID-19: A Literature Review

Cited by 25 publications

References 131 publications

Endothelial dysfunction in COVID-19: an overview of evidence, biomarkers, mechanisms and potential therapies

Endothelial dysfunction in COVID-19: an overview of evidence, biomarkers, mechanisms and potential therapies

Effect of coronaviruses on blood vessel permeability: potential therapeutic targets

Rap1 small GTPase is essential for maintaining pulmonary endothelial barrier function in mice

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