Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10586890 | PMC |
| http://dx.doi.org/10.1055/a-2156-8048 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Complement System and Adhesion Molecule Skirmishes in Fabry Disease: Insights into Pathogenesis and Disease Mechanisms.
Int J Mol Sci
November 2024
Division of Human Genetics, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Fabry disease is a rare X-linked lysosomal storage disorder caused by mutations in the galactosidase alpha () gene, resulting in the accumulation of globotriaosylceramide (Gb3) and its deacetylated form, globotriaosylsphingosine (Lyso-Gb3) in various tissues and fluids throughout the body. This pathological accumulation triggers a cascade of processes involving immune dysregulation and complement system activation. Elevated levels of complement 3a (C3a), C5a, and their precursor C3 are observed in the plasma, serum, and tissues of patients with Fabry disease, correlating with significant endothelial cell abnormalities and vascular dysfunction.
View Article and Find Full Text PDFActivation of platelets and the complement system in mice with -induced pulmonary hypertension.
Am J Physiol Lung Cell Mol Physiol
November 2024
Section of Neonatology, Department of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States.
Schistosomiasis-induced pulmonary hypertension (PH) presents a significant global health burden, yet the underlying mechanisms remain poorly understood. Here, we investigate the involvement of platelets and the complement system in the initiation events leading to -induced PH. We demonstrate that exposure leads to thrombocytopenia, platelet accumulation in the lung, and platelet activation.
View Article and Find Full Text PDFThe Platelet Anaphylatoxin Receptor C5aR1 (CD88) Is a Promising Target for Modulating Vessel Growth in Response to Ischemia .
TH Open
October 2023
Cardioimmunology Group, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany.
SARS-CoV-2 spike protein induces lung endothelial cell dysfunction and thrombo-inflammation depending on the C3a/C3a receptor signalling.
Sci Rep
July 2023
Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo, Italy.
The spike protein of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) can interact with endothelial cells. However, no studies demonstrated the direct effect of the spike protein subunit 1 (S1) in inducing lung vascular damage and the potential mechanisms contributing to lung injury. Here, we found that S1 injection in mice transgenic for human angiotensin converting enzyme 2 (ACE2) induced early loss of lung endothelial thromboresistance at 3 days, as revealed by thrombomodulin loss and von Willebrand factor (vWF) increase.
View Article and Find Full Text PDFComplement and platelets: prothrombotic cell activation requires membrane attack complex-induced release of danger signals.
Blood Adv
October 2023
Institute of Experimental and Clinical Pharmacology, Toxicology and Pharmacology of Natural Products, University of Ulm Medical Center, Ulm, Germany.
Complement activation in the diseases paroxysmal nocturnal hemoglobinuria (PNH) and atypical hemolytic uremic syndrome (aHUS) results in cytolysis and fatal thrombotic events, which are largely refractory to anticoagulation and/or antiplatelet therapy. Anticomplement therapy, however, efficiently prevents thrombotic events in PNH and aHUS, but the underlying mechanisms remain unresolved. We show that complement-mediated hemolysis in whole blood induces platelet activation similarly to activation by adenosine 5'-diphosphate (ADP).
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!