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

Acta Pharmacologica Sinica, Journal Year: 2022, Volume and Issue: 44(4), P. 695 - 709

Published: Oct. 17, 2022

Language: Английский

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Long COVID endotheliopathy: hypothesized mechanisms and potential therapeutic approaches

Journal of Clinical Investigation, Journal Year: 2022, Volume and Issue: 132(15)

Published: July 31, 2022

SARS-CoV-2–infected individuals may suffer a multi–organ system disorder known as "long COVID" or post-acute sequelae of SARS-CoV-2 infection (PASC). There are no standard treatments, the pathophysiology is unknown, and incidence varies by clinical phenotype. Acute COVID-19 correlates with biomarkers systemic inflammation, hypercoagulability, comorbidities that less prominent in PASC. Macrovessel thrombosis, hallmark acute COVID-19, frequent Female sex at birth associated reduced risk for progression, but increased Persistent microvascular endotheliopathy cryptic tissue reservoirs has been implicated PASC pathology. Autoantibodies, localized reactivation latent pathogens also be involved, potentially leading to documented multiple tissues. Diagnostic assays illuminating possible therapeutic targets discussed.

Language: Английский

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Long COVID: The Nature of Thrombotic Sequelae Determines the Necessity of Early Anticoagulation

Frontiers in Cellular and Infection Microbiology, Journal Year: 2022, Volume and Issue: 12

Published: April 5, 2022

Many discharged COVID-19 patients affected by sequelae experience reduced quality of life leading to an increased burden on the healthcare system, their families and society at large. Possible pathophysiological mechanisms long COVID include: persistent viral replication, chronic hypoxia inflammation. Ongoing vascular endothelial damage promotes platelet adhesion coagulation, resulting in impairment various organ functions. Meanwhile, thrombosis will further aggravate vasculitis contributing deterioration. Thus, is essentially a thrombotic sequela. Unfortunately, there currently no effective treatment for COVID. This article summarizes evidence coagulation abnormalities COVID, with focus thrombosis. Extracellular vesicles (EVs) released types cells can carry SARS-CoV-2 through circulation attack distant tissues organs. Furthermore, EVs express tissue factor phosphatidylserine (PS) which Given persistence virus, inflammation are inevitable. Pulmonary structural changes such as hypertension, embolism fibrosis common The impaired lung function again aggravates abnormalities. In this article, we also summarize recent research antithrombotic therapy COVID-19. There increasing that early anticoagulation be improving outcomes. fact, systemic dysfunction caused key factors driving complications Early prophylactic prevent release or remove procoagulant substances, thereby protecting endothelium from damage, reducing sequelae, long-COVID patients.

Language: Английский

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Long-Term Outcomes of Pediatric Infections: From Traditional Infectious Diseases to Long Covid

Future Microbiology, Journal Year: 2022, Volume and Issue: 17(7), P. 551 - 571

Published: March 10, 2022

There is limited evidence available on the long-term impact of SARS-CoV-2 infection in children. In this article, authors analyze recent pediatric long Covid and lessons learnt from a post-Covid unit Rome, Italy. To gain better understanding concerns raised by parents physicians relation to potential consequences novel infection, it important recognize that effect post-infectious disease not new phenomenon.

Language: Английский

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COVID-19 Causes Ferroptosis and Oxidative Stress in Human Endothelial Cells

Antioxidants, Journal Year: 2023, Volume and Issue: 12(2), P. 326 - 326

Published: Jan. 31, 2023

Oxidative stress and endothelial dysfunction have been shown to play crucial roles in the pathophysiology of COVID-19 (coronavirus disease 2019). On these grounds, we sought investigate impact on lipid peroxidation ferroptosis human cells. We hypothesized that oxidative induced by cells could be linked outcome. Thus, collected serum from patients hospital admission, incubated sera with cells, comparing effects generation reactive oxygen species (ROS) between who survived did not survive. found non-survivors significantly increased peroxidation. Moreover, markedly regulated expression levels main markers ferroptosis, including GPX4, SLC7A11, FTH1, SAT1, a response was rescued silencing TNFR1 Taken together, our data indicate survive triggers

Language: Английский

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Damage to endothelial barriers and its contribution to long COVID

Angiogenesis, Journal Year: 2023, Volume and Issue: 27(1), P. 5 - 22

Published: April 27, 2023

Language: Английский

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Pathophysiological mechanisms of thrombosis in acute and long COVID-19

Frontiers in Immunology, Journal Year: 2022, Volume and Issue: 13

Published: Nov. 16, 2022

COVID-19 patients have a high incidence of thrombosis, and thromboembolic complications are associated with severe mortality. disease is hyper-inflammatory response (cytokine storm) mediated by the immune system. However, role inflammatory in thrombosis remains incompletely understood. In this review, we investigate crosstalk between inflammation context COVID-19, focusing on contributions to pathogenesis propose combined use anti-inflammatory anticoagulant therapeutics. Under conditions, interactions neutrophils platelets, platelet activation, monocyte tissue factor expression, microparticle release, phosphatidylserine (PS) externalization as well complement activation collectively involved immune-thrombosis. Inflammation results apoptosis blood cells, leading release PS cells microparticles, which significantly enhances catalytic efficiency tenase prothrombinase complexes, promotes thrombin-mediated fibrin generation local clot formation. Given risk importance antithrombotic therapies has been generally recognized, but certain deficiencies treatment gaps remain. Antiplatelet drugs not combination treatments, thus fail dampen procoagulant activity. Current treatments also do an optimal time for anticoagulation. The efficacy depends therapy initiation. best early possible after diagnosis, ideally stage disease. We elaborate mechanisms long COVID complications, including persistent inflammation, endothelial injury dysfunction, coagulation abnormalities. above-mentioned contents provide therapeutic strategies further improve patient outcomes.

Language: Английский

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Beyond Acute COVID-19: A Review of Long-term Cardiovascular Outcomes

Canadian Journal of Cardiology, Journal Year: 2023, Volume and Issue: 39(6), P. 726 - 740

Published: Feb. 6, 2023

Statistics Canada estimated that approximately 1.4 million Canadians suffer from long COVID. Although cardiovascular changes during acute SARS-CoV-2 infection are well documented, long-term sequelae less understood. In this review, we sought to characterize adult outcomes in the months after COVID-19 illness. our search identified reports of including cardiac dysautonomia, myocarditis, ischemic injuries, and ventricular dysfunction. Even patients without overt outcomes, subclinical have been observed. Cardiovascular can stem exacerbation preexisting conditions, ongoing inflammation, or as a result damage occurred infection. For example, myocardial fibrosis has reported hospital admission for illness, might be consequence myocarditis injury disease. turn, contribute further dysrhythmias heart failure. Severity risk factor consequences, however, also young, healthy individuals who had asymptomatic mild evolving evidence suggests previous disease, there is heterogeneity existing evidence, some studies marred by measured unmeasured confounders. Many investigations limited relatively short follow-up. Future should focus on longer term (beyond 1 year) identifying prevalence different populations basis COVID disease severity.

Language: Английский

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Microvascular Thrombosis as a Critical Factor in Severe COVID-19

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(3), P. 2492 - 2492

Published: Jan. 27, 2023

Platelet-endothelial interactions have a critical role in microcirculatory function, which maintains tissue homeostasis. The subtle equilibrium between platelets and the vessel wall is disturbed by coronavirus disease 2019 (COVID-19), affects all three components of Virchow's triad (endothelial injury, stasis hypercoagulable state). Endotheliitis, vasculitis, glycocalyx degradation, alterations blood flow viscosity, neutrophil extracellular trap formation microparticle shedding are only few pathomechanisms contributing to endothelial damage microthrombosis resulting capillary plugging ischemia. In following opinion paper, we discuss major pathological processes leading microvascular activation thrombosis as possible adverse factor driving deterioration patient course severe COVID-19.

Language: Английский

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Vascular Alterations Following COVID-19 Infection: A Comprehensive Literature Review

Life, Journal Year: 2024, Volume and Issue: 14(5), P. 545 - 545

Published: April 24, 2024

SARS-CoV-2, the causative agent of ongoing COVID-19 pandemic, has revealed a broader impact beyond respiratory system, predominantly affecting vascular system with various adverse manifestations. The infection induces endothelial dysfunction and immune dysregulation, creating an inflammatory hypercoagulable state. It affects both microvasculature macrovasculature, leading to thromboembolic events, cardiovascular manifestations, impaired arterial stiffness, cerebrovascular complications, nephropathy, as well retinopathy-frequently observed in cases severe illness. Evidence suggests that SARS-CoV-2 may result persistent effects on identified long-term COVID-19. This is characterized by prolonged inflammation, endotheliopathy, increased risk complications. Various imaging modalities, histopathological studies, diagnostic tools such video capillaroscopy magnetic resonance have been employed visualize alterations. review aims comprehensively summarize evidence concerning short alterations following infection, investigating their patients' prognosis, providing overview preventive strategies mitigate associated

Language: Английский

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