Endothelial Damage in Acute Respiratory Distress Syndrome

Abstract

The pulmonary endothelium is a metabolically active continuous monolayer of squamous endothelial cells that internally lines blood vessels and mediates key processes involved in lung homoeostasis. Many of these processes are disrupted in acute respiratory distress syndrome (ARDS), which is marked among others by diffuse endothelial injury, intense activation of the coagulation system and increased capillary permeability. Most commonly occurring in the setting of sepsis, ARDS is a devastating illness, associated with increased morbidity and mortality and no effective pharmacological treatment. Endothelial cell damage has an important role in the pathogenesis of ARDS and several biomarkers of endothelial damage have been tested in determining prognosis. By further understanding the endothelial pathobiology, development of endothelial-specific therapeutics might arise. In this review, we will discuss the underlying pathology of endothelial dysfunction leading to ARDS and emerging therapies. Furthermore, we will present a brief overview demonstrating that endotheliopathy is an important feature of hospitalised patients with coronavirus disease-19 (COVID-19).

ICU Admission Levels of Endothelial Biomarkers as Predictors of Mortality in Critically Ill COVID-19 Patients

“…Given the high mortality rates in these patients, however, early identification of prognostic indicators is crucial. Endothelial dysfunction has been shown to be directly involved in ARDS and sepsis [ 16 ], however its involvement in COVID-19 is being currently explored [ 17 ]. Markers of endothelial activation and dysfunction could be studied for increased risk of COVID-19-associated mortality.…”

COVID-19-associated acute respiratory distress syndrome (CARDS): Current knowledge on pathophysiology and ICU treatment – A narrative review

“…Pooled mortality among patients with vs. without thromboembolic events was 23% (95% CI: 14%–32%) vs. 13% (95% CI: 6%–22%) [ 71 ]. Although the exact underlying pathophysiology that leads to COVID-19-associated coagulopathy is not fully understood, it appears that endotheliopathy, vasoocclusion/stasis, and inflammation-associated activation of coagulation contribute to the respective complications [ [72] , [73] , [74] ].…”

Clinical management of patients with rheumatoid arthritis during the COVID-19 pandemic

“…Pathogenesis of both ILD-AE and ARDS is poorly understood but both involve hyperinflammation, mainly driven by T helper 1 and M1 machrophages, characterized by secretion of proinflammatory cytokines, such as TNFα, IL-6, and IL-12, extracellular matrix destruction, and apoptosis [40,42]. Moreover, the excessive inflammatory response promotes an hypercoagulable state, directly, or indirectly through endothelial damage [43].…”