COVID-19 acute respiratory distress syndrome: can iloprost have a role for the treatment?

Filippini, Alida; Bnà, Claudio; Bellosta, Raffaello; Bazzani, Roberto; Luzzani, Luca; Pegorer, Matteo; Zandalasini, Matteo; Baldon, Michela; Codazzi, Manuela; Sabatini, Tony

doi:10.1016/j.rmcr.2021.101358

Cited by 4 publications

(4 citation statements)

References 19 publications

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“…The prostacyclin (PGI2) analogue, iloprost, showed beneficial effects in COVID-19 patients. Iloprost might represent a valuable therapeutic option for respiratory performance improvement [124]. Synthesized in the vascular endothelium, PGI2 plays a role not only in the endothelial barrier homeostasis and platelet aggregation, but it also has anti-inflammatory and vasodilatory effects.…”

Section: Therapeutic Targets For the Treatment Of Covid-19mentioning

confidence: 99%

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Endothelial Dysfunction, Inflammation, and Oxidative Stress in COVID-19—Mechanisms and Therapeutic Targets

Fodor

Tiperciuc

et al. 2021

Oxidative Medicine and Cellular Longevity

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The outbreak of the COVID-19 pandemic represents an ongoing healthcare emergency responsible for more than 3.4 million deaths worldwide. COVID-19 is the disease caused by SARS-CoV-2, a virus that targets not only the lungs but also the cardiovascular system. COVID-19 can manifest with a wide range of clinical manifestations, from mild symptoms to severe forms of the disease, characterized by respiratory failure due to severe alveolar damage. Several studies investigated the underlying mechanisms of the severe lung damage associated with SARS-CoV-2 infection and revealed that the respiratory failure associated with COVID-19 is the consequence not only of acute respiratory distress syndrome but also of macro- and microvascular involvement. New observations show that COVID-19 is an endothelial disease, and the consequent endotheliopathy is responsible for inflammation, cytokine storm, oxidative stress, and coagulopathy. In this review, we show the central role of endothelial dysfunction, inflammation, and oxidative stress in the COVID-19 pathogenesis and present the therapeutic targets deriving from this endotheliopathy.

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Section: Therapeutic Targets For the Treatment Of Covid-19mentioning

confidence: 99%

“…In COVID-19 patients, iloprost could prevent the associated thrombotic events through its protective effects on the endothelium and the antithrombotic activity [124]. 6.10.…”

Section: Therapeutic Targets For the Treatment Of Covid-19mentioning

confidence: 99%

Endothelial Dysfunction, Inflammation, and Oxidative Stress in COVID-19—Mechanisms and Therapeutic Targets

Fodor

Tiperciuc

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…Unexpectedly, this also resulted in an improvement in respiratory symptoms, and high-resolution computed tomography of the lung showed significant regression of diffuse pulmonary ground-glass opacity. Results suggest that iloprost could have potential for treating COVID-19 [ 110 ].…”

Section: Covid-19-associated Changes In Serum Glycerophospholipids An...mentioning

confidence: 99%

COVID-19, Blood Lipid Changes, and Thrombosis

Farooqui

Sun

et al. 2023

Biomedicines

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Although there is increasing evidence that oxidative stress and inflammation induced by COVID-19 may contribute to increased risk and severity of thromboses, the underlying mechanism(s) remain to be understood. The purpose of this review is to highlight the role of blood lipids in association with thrombosis events observed in COVID-19 patients. Among different types of phospholipases A2 that target cell membrane phospholipids, there is increasing focus on the inflammatory secretory phospholipase A2 IIA (sPLA2-IIA), which is associated with the severity of COVID-19. Analysis indicates increased sPLA2-IIA levels together with eicosanoids in the sera of COVID patients. sPLA2 could metabolise phospholipids in platelets, erythrocytes, and endothelial cells to produce arachidonic acid (ARA) and lysophospholipids. Arachidonic acid in platelets is metabolised to prostaglandin H2 and thromboxane A2, known for their pro-coagulation and vasoconstrictive properties. Lysophospholipids, such as lysophosphatidylcholine, could be metabolised by autotaxin (ATX) and further converted to lysophosphatidic acid (LPA). Increased ATX has been found in the serum of patients with COVID-19, and LPA has recently been found to induce NETosis, a clotting mechanism triggered by the release of extracellular fibres from neutrophils and a key feature of the COVID-19 hypercoagulable state. PLA2 could also catalyse the formation of platelet activating factor (PAF) from membrane ether phospholipids. Many of the above lipid mediators are increased in the blood of patients with COVID-19. Together, findings from analyses of blood lipids in COVID-19 patients suggest an important role for metabolites of sPLA2-IIA in COVID-19-associated coagulopathy (CAC).

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“…Moreover, prostacyclin protects the endothelium and the endothelial glycocalyx, and has anti-inflammatory effects [ 98 , 99 , 100 , 101 , 102 , 103 , 104 , 105 ]. The prostacyclin analogue iloprost has shown beneficial effects in patients with COVID-19 through its ability to protect the endothelium and its antithrombotic activity [ 106 ]. In adults with COVID-19 requiring mechanical ventilation and who had a plasma thrombomodulin level >4 ng/mL, a 72 h infusion of prostacyclin (1 ng/kg/min) was associated with a longer median 28-day survival time without mechanical ventilation (16 days vs. 5 days in the placebo group).…”

Section: Covid-19 Treatments That Target the Endothelium Or Endotheli...mentioning

confidence: 99%

The Endothelium and COVID-19: An Increasingly Clear Link Brief Title: Endotheliopathy in COVID-19

Six

Guillaume

Jacob

et al. 2022

IJMS

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The endothelium has a fundamental role in the cardiovascular complications of coronavirus disease 2019 (COVID-19). Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) particularly affects endothelial cells. The virus binds to the angiotensin-converting enzyme 2 (ACE-2) receptor (present on type 2 alveolar cells, bronchial epithelial cells, and endothelial cells), and induces a cytokine storm. The cytokines tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 have particular effects on endothelial cells—leading to endothelial dysfunction, endothelial cell death, changes in tight junctions, and vascular hyperpermeability. Under normal conditions, apoptotic endothelial cells are removed into the bloodstream. During COVID-19, however, endothelial cells are detached more rapidly, and do not regenerate as effectively as usual. The loss of the endothelium on the luminal surface abolishes all of the vascular responses mediated by the endothelium and nitric oxide production in particular, which results in greater contractility. Moreover, circulating endothelial cells infected with SARS-CoV-2 act as vectors for viral dissemination by forming clusters that migrate into the circulation and reach distant organs. The cell clusters and the endothelial dysfunction might contribute to the various thromboembolic pathologies observed in COVID-19 by inducing the formation of intravascular microthrombi, as well as by triggering disseminated intravascular coagulation. Here, we review the contributions of endotheliopathy and endothelial-cell-derived extracellular vesicles to the pathogenesis of COVID-19, and discuss therapeutic strategies that target the endothelium in patients with COVID-19.

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COVID-19 acute respiratory distress syndrome: can iloprost have a role for the treatment?

Cited by 4 publications

References 19 publications

Endothelial Dysfunction, Inflammation, and Oxidative Stress in COVID-19—Mechanisms and Therapeutic Targets

Endothelial Dysfunction, Inflammation, and Oxidative Stress in COVID-19—Mechanisms and Therapeutic Targets

COVID-19, Blood Lipid Changes, and Thrombosis

The Endothelium and COVID-19: An Increasingly Clear Link Brief Title: Endotheliopathy in COVID-19

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