Cited by Human herpesvirus reactivation and its potential role in the pathogenesis of post-acute sequelae of SARS-CoV-2 infection

Mechanisms of endothelial activation, hypercoagulation and thrombosis in COVID-19: a link with diabetes mellitus DOI

Inés Valencia, Jairo Lumpuy‐Castillo, Giselle Santos Magalhães

et al.

Cardiovascular Diabetology, Journal Year: 2024, Volume and Issue: 23(1)

Published: Feb. 20, 2024

Abstract Early since the onset of COVID-19 pandemic, medical and scientific community were aware extra respiratory actions SARS-CoV-2 infection. Endothelitis, hypercoagulation, hypofibrinolysis identified in patients as subsequent responses endothelial dysfunction. Activation barrier may increase severity disease contribute to long-COVID syndrome post-COVID sequelae. Besides, it cause alterations primary, secondary, tertiary hemostasis. Importantly, these have been highly decisive evolution infected also diagnosed with diabetes mellitus (DM), who showed previous In this review, we provide an overview potential triggers activation related under diabetic milieu. Several mechanisms are induced by both viral particle itself immune-defensive response (i.e., NF-κB/NLRP3 inflammasome pathway, vasoactive peptides, cytokine storm, NETosis, complement system). Alterations coagulation mediators such factor VIII, fibrin, tissue factor, von Willebrand factor: ADAMST-13 ratio, kallikrein-kinin or plasminogen-plasmin systems reported. Moreover, imbalance thrombotic thrombolytic (tPA, PAI-I, fibrinogen) factors favors hypercoagulation hypofibrinolysis. context DM, can be exacerbated leading higher loss However, a series therapeutic strategies targeting activated endothelium specific antibodies inhibitors against thrombin, key cytokines, X, system, system might represent new opportunities address hypercoagulable state present DM. Antidiabetics ameliorate dysfunction, inflammation, platelet aggregation. By improving microvascular pathology subjects, associated comorbidities risk mortality could reduced.

Language: Английский

Citations

Pathophysiological, immunological, and inflammatory features of long COVID DOI

Karen Böhmwald, Benjamín Diethelm‐Varela,

Linmar Rodríguez-Guilarte

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Feb. 28, 2024

The COVID-19 pandemic continues to cause severe global disruption, resulting in significant excess mortality, overwhelming healthcare systems, and imposing substantial social economic burdens on nations. While most of the attention therapeutic efforts have concentrated acute phase disease, a notable proportion survivors experience persistent symptoms post-infection clearance. This diverse set symptoms, loosely categorized as long COVID, presents potential additional public health crisis. It is estimated that 1 5 exhibit clinical manifestations consistent with COVID. Despite this prevalence, mechanisms pathophysiology COVID remain poorly understood. Alarmingly, evidence suggests cases within condition develop debilitating or disabling symptoms. Hence, urgent priority should be given further studies equip systems for its management. review provides an overview available information emerging condition, focusing affected individuals’ epidemiology, pathophysiological mechanisms, immunological inflammatory profiles.

Language: Английский

Citations

Cerebromicrovascular mechanisms contributing to long COVID: implications for neurocognitive health DOI

Mónika Fekete, Andrea Ceglédi,

Ágnes Szappanos

et al.

GeroScience, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 7, 2025

Abstract Long COVID (also known as post-acute sequelae of SARS-CoV-2 infection [PASC] or post-COVID syndrome) is characterized by persistent symptoms that extend beyond the acute phase infection, affecting approximately 10% to over 30% those infected. It presents a significant clinical challenge, notably due pronounced neurocognitive such brain fog. The mechanisms underlying these effects are multifactorial, with mounting evidence pointing central role cerebromicrovascular dysfunction. This review investigates key pathophysiological contributing cerebrovascular dysfunction in long and their impacts on health. We discuss how endothelial tropism direct vascular trigger dysfunction, impaired neurovascular coupling, blood–brain barrier disruption, resulting compromised cerebral perfusion. Furthermore, appears induce mitochondrial enhancing oxidative stress inflammation within cells. Autoantibody formation following also potentially exacerbates injury, chronic ongoing compromise. These factors collectively contribute emergence white matter hyperintensities, promote amyloid pathology, may accelerate neurodegenerative processes, including Alzheimer’s disease. emphasizes critical advanced imaging techniques assessing health need for targeted interventions address complications. A deeper understanding essential advance treatments mitigate its long-term consequences.

Language: Английский

Citations

Long COVID-19 Pathophysiology: What Do We Know So Far? DOI

Nikolaos Tziolos, Πέτρος Ιωάννου, Stella Baliou

et al.

Microorganisms, Journal Year: 2023, Volume and Issue: 11(10), P. 2458 - 2458

Published: Sept. 30, 2023

Long COVID-19 is a recognized entity that affects millions of people worldwide. Its broad clinical symptoms include thrombotic events, brain fog, myocarditis, shortness breath, fatigue, muscle pains, and others. Due to the binding virus with ACE-2 receptors, expressed in many organs, it can potentially affect any system; however, most often cardiovascular, central nervous, respiratory, immune systems. Age, high body mass index, female sex, previous hospitalization, smoking are some its risk factors. Despite great efforts define pathophysiology, gaps remain be explained. The main mechanisms described literature involve viral persistence, hypercoagulopathy, dysregulation, autoimmunity, hyperinflammation, or combination these. exact may differ from system system, but share same pathways. This review aims describe prevalent pathophysiological pathways explaining this syndrome.

Language: Английский

Citations

Exploring the Pathophysiology of Long COVID: The Central Role of Low-Grade Inflammation and Multisystem Involvement DOI

Evgeni Gusev, Alexey Sarapultsev

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(12), P. 6389 - 6389

Published: June 9, 2024

Long COVID (LC), also referred to as Post COVID-19 Condition, Post-Acute Sequelae of SARS-CoV-2 Infection (PASC), and other terms, represents a complex multisystem disease persisting after the acute phase COVID-19. Characterized by myriad symptoms across different organ systems, LC presents significant diagnostic management challenges. Central disorder is role low-grade inflammation, non-classical inflammatory response that contributes chronicity diversity observed. This review explores pathophysiological underpinnings LC, emphasizing importance inflammation core component. By delineating pathogenetic relationships clinical manifestations this article highlights necessity for an integrated approach employs both personalized medicine standardized protocols aimed at mitigating long-term consequences. The insights gained not only enhance our understanding but inform development therapeutic strategies could be applicable chronic conditions with similar features.

Language: Английский

Citations

Endothelial dysfunction and persistent inflammation in severe post-COVID-19 patients: implications for gas exchange DOI

Enrique Alfaro, Elena Díaz‐García,

Sara García-Tovar

et al.

BMC Medicine, Journal Year: 2024, Volume and Issue: 22(1)

Published: June 13, 2024

Abstract Background Understanding the enduring respiratory consequences of severe COVID-19 is crucial for comprehensive patient care. This study aims to evaluate impact post-COVID conditions on sequelae acute distress syndrome (ARDS). Methods We examined 88 survivors COVID-19-associated ARDS six months post-intensive care unit (ICU) discharge. Assessments included clinical and functional evaluation as well plasma biomarkers endothelial dysfunction, inflammation, viral response. Additionally, an in vitro model using human umbilical vein cells (HUVECs) explored direct function. Results Post-COVID patients with impaired gas exchange demonstrated persistent inflammation marked by elevated ICAM-1, IL-8, CCL-2, ET-1 levels. Concurrently, systemic evidenced NLRP3 overexpression levels IL-6, sCD40-L, C-reactive protein, was associated dysfunction increased exchange. T-cell activation, reflected CD69 expression, persistently interferon-β (IFN-β) further contributed sustained inflammation. The confirmed that plasma, altered sCD40-L IFN-β proteins, has capacity alter Conclusions Six post-ICU discharge, exhibited elevation biomarkers, correlating severity inflammasome activity activation indicate going contributing potentially intensified immune

Language: Английский

Citations

The role of atrial fibrillation in vascular cognitive impairment and dementia: epidemiology, pathophysiology, and preventive strategies DOI

Mónika Fekete, Eric M. Liotta, Tihamér Molnár

et al.

GeroScience, Journal Year: 2024, Volume and Issue: unknown

Published: Aug. 13, 2024

The aging population in Europe faces a substantial burden from dementia, with vascular cognitive impairment and dementia (VCID) being preventable cause. Atrial fibrillation (AF), common cardiac arrhythmia, increases the risk of VCID through mechanisms such as thromboembolism, cerebral hypoperfusion, inflammation. This review explores epidemiology, pathophysiology, preventive strategies for AF-related VCID. Epidemiological data indicate that AF prevalence rises age, affecting up to 12% individuals over 80. Neuroimaging studies reveal chronic brain changes patients, including strokes, lacunar white matter hyperintensities (WMHs), microbleeds (CMHs), while assessments show impairments memory, executive function, attention. COVID-19 pandemic has exacerbated underdiagnosis AF, leading an increase undiagnosed strokes impairment. Many elderly did not seek medical care due fear exposure, resulting delayed diagnoses. Additionally, reduced family supervision during contributed missed opportunities early detection related complications. Emerging evidence suggests long COVID may also elevate further complicating management this condition. underscores importance comprehensive mitigate decline. Preventive measures, public awareness campaigns, patient education, use smart devices detection, are crucial. Anticoagulation therapy, rate rhythm control, addressing comorbid conditions essential therapeutic strategies. Recognizing cardiovascular impacts especially context pandemic, is advancing health.

Language: Английский

Citations

Observational Study of Repeat Immunoadsorption (RIA) in Post-COVID ME/CFS Patients with Elevated ß2-Adrenergic Receptor Autoantibodies—An Interim Report DOI

Elisa Stein,

Cornelia Heindrich, Kirsten Wittke

et al.

Journal of Clinical Medicine, Journal Year: 2023, Volume and Issue: 12(19), P. 6428 - 6428

Published: Oct. 9, 2023

There is increasing evidence for an autoimmune aetiology in post-infectious Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). SARS-CoV-2 has now become the main trigger ME/CFS. We have already conducted two small proof-of-concept studies on IgG depletion by immunoadsorption (IA) ME/CFS, which showed efficacy most patients. This observational study aims to evaluate of IA patients with post-COVID-19 The primary objective was assess improvement functional ability. Due urgency finding therapies post-COVID-Syndrome (PCS), we report here interim results first ten patients, seven responders defined increase between 10 and 35 points Short-Form 36 Physical Function (SF36-PF) at week four after IA. this will provide basis patient selection a randomised controlled trial (RCT), including sham apheresis, RCT combining B-cell therapy. Trial registration number: NCT05629988.

Language: Английский

Citations

Long COVID as a Disease of Accelerated Biological Aging: An Opportunity to Translate Geroscience Interventions DOI

Areez Shafqat, Mary Clare Masters, Utkarsh Tripathi

et al.

Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 99, P. 102400 - 102400

Published: June 28, 2024

Language: Английский

Citations

SARS-CoV-2 S Protein Reduces Cytoprotective Defenses and Promotes Human Endothelial Cell Senescence DOI

Alicia Villacampa, Licia Shamoon, Inés Valencia

et al.

Aging and Disease, Journal Year: 2024, Volume and Issue: unknown, P. 0 - 0

Published: Jan. 1, 2024

Premature vascular aging and endothelial cell senescence are major risk factors for cardiovascular diseases atherothrombotic disturbances, which main complications of both acute long COVID-19. The S protein SARS-CoV2, acts as the receptor binding viral infection, is able to induce cells inflammation it has been found an isolated element in circulation human tissues reservoirs months after infection. Here, we investigated whether directly deciphered some mechanisms involved. In primary cultures umbilical vein (HUVEC), SARS-CoV-2 enhanced a concentration-dependent manner cellular content DNA damage response markers (senescence-associated-β galactosidase, γH2AX), well growth-arrest effectors (p53, p21, p16). parallel, reduced availability cytoprotective proteins, such anti-aging klotho, Nrf2 or heme oxygenase-1, caused functional harm by impairing ex vivo endothelial-dependent vasorelaxation murine microvessels. These effects were prevented pharmacological inhibition NLRP3 inflammasome with MCC950. Furthermore, supplementation either recombinant klotho angiotensin-(1-7), equally protected against pro-senescence, pro-inflammatory pro-oxidant action protein. Globally, this study proposes novel disease context COVID-19 its sequelae provides clues order prevent complications.

Language: Английский

Citations