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The world is in a hard battle against COVID-19. Endothelial cells are among the most critical targets of SARS-CoV-2. Dysfunction of endothelium leads to vascular injury following by coagulopathies and thrombotic conditions in the vital organs increasing the risk of life-threatening events. Growing evidences revealed that endothelial dysfunction and consequent thrombotic conditions are associated with the severity of outcomes. It is not yet fully clear that these devastating sequels originate directly from the virus or a side effect of virus-induced cytokine storm. Due to endothelial dysfunction, plasma levels of some biomarkers are changed and relevant clinical manifestations appear as well. Stabilization of endothelial integrity and supporting its function are among the promising therapeutic strategies. Other than respiratory, COVID-19 could be called a systemic vascular disease and this aspect should be scrutinized in more detail in order to reduce related mortality. In the present investigation, the effects of COVID-19 on endothelial function and thrombosis formation are discussed. In this regard, critical players, laboratory findings, clinical manifestation, and suggestive therapies are presented.
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http://dx.doi.org/10.1177/10760296211042940 | DOI Listing |
Eur J Case Rep Intern Med
August 2025
Nephrology Department, Unidade Local de Saúde de Braga, Braga, Portugal.
Introduction: Bevacizumab is a monoclonal antibody that targets vascular endothelial growth factor (VEGF) and is widely used in oncology for its anti-angiogenic properties. However, VEGF inhibition may result in significant nephrotoxicity, including thrombotic microangiopathy (TMA). While systemic TMA is well-described, isolated renal-limited TMA remains under recognised.
View Article and Find Full Text PDFMater Today Bio
October 2025
Department of Vascular Surgery, The Affiliated Hospital of Southwest Medical University, 646000, Luzhou, China.
Atherosclerosis (AS) is a chronic inflammatory disease driven by endothelial dysfunction, vascular smooth muscle cell proliferation, and insufficient resolution of inflammation. Nitric oxide (NO) plays a crucial role in vascular homeostasis by promoting endothelial cell proliferation, maintaining endothelial integrity, suppressing smooth muscle cell hyperplasia, and exerting potent anti-inflammatory effects. However, clinical application of NO is hindered by its short half-life, lack of targeting, and uncontrolled release.
View Article and Find Full Text PDFClin Kidney J
September 2025
Hypertension is a pervasive and progressive complication in chronic kidney disease (CKD) patients, affecting up to 90% of those in advanced stages or on dialysis. A particularly insidious aspect of this condition is nocturnal hypertension, characterized by high blood pressure (BP) during sleep and a blunted or absent nighttime BP dipping-phenomena associated with accelerated CKD progression and increased cardiovascular risk. Despite its strong prognostic significance, nocturnal hypertension remains underdiagnosed due to limited use of ambulatory BP monitoring.
View Article and Find Full Text PDFVasc Health Risk Manag
September 2025
Department of Functional Diagnostics and Physical Medicine, Pomeranian Medical University in Szczecin, Szczecin, 71-210, Poland.
The vascular endothelium is responsible for regulating vascular tone, maintaining fluid homeo-stasis, and preventing platelet aggregation, exhibits regulatory properties in vasorelaxation and vasoconstriction - it produces, among others, nitric oxide and endothelin. The imbalance of vasoactive molecules leads to the loss of their function, known as endothelial dysfunction. Impaired endothelial function is observed in people with metabolic disorders, often preceding the onset of the disease by several years.
View Article and Find Full Text PDFRev Cardiovasc Med
August 2025
Department of Nephrology, Akron Nephrology Associates at Cleveland Clinic Akron General Medical Center, Akron, OH 44302, USA.
Cardiovascular assessments in children and adolescents with hypertension are essential for detecting early signs of organ damage and guiding timely interventions. The pathophysiology of pediatric hypertension involves a complex interplay of arterial stiffness, endothelial dysfunction, metabolic disturbances, activation of the renin-angiotensin-aldosterone system, and immune dysregulation. These mechanisms collectively contribute to target organ damage, particularly in the cardiovascular system.
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