Publications by authors named "S K Naveenkumar"
Platelets are essential for normal hemostasis and thrombosis but become hyperactive in hemolytic disorders. Cell-free heme is known to be toxic to platelets and endothelial cells, playing a significant role in the progression of pathological complications in various hemolytic conditions. The abnormal activation of circulatory platelets results in micro/macrovascular thrombosis and clot formation in the lungs, worsening the disease.
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- Neutrophil hyperactivity and NET release are key factors in the autoimmune disease antiphospholipid syndrome (APS).
- Research shows that neutrophils from APS patients have a higher reliance on glycolysis compared to those from healthy individuals, particularly in cases linked to microvascular disease.
- Inhibiting glycolysis or the pentose phosphate pathway (PPP) not only reduces NET release and reactive oxygen species production in neutrophils but also significantly decreases thrombosis in mice models of APS.
Our study aimed to evaluate the presence, clinical associations, and potential mechanistic roles of non-criteria antiphospholipid antibodies (aPL) and circulating calprotectin, a highly stable marker of neutrophil extracellular trap release (NETosis), in pediatric APS patients. We found that 79% of pediatric APS patients had at least one non-criteria aPL at moderate-to-high titer. Univariate logistic regression demonstrated that positive anti-beta-2 glycoprotein I domain 1 (anti-D1) IgG (p = 0.
View Article and Find Full Text PDFMany patients with antiphospholipid syndrome had decreased ectonucleotidase activity on neutrophils and platelets, which enabled extracellular nucleotides to trigger neutrophil-platelet aggregates. This phenotype was replicated by treating healthy neutrophils and platelets with patient-derived antiphospholipid antibodies or ectonucleotidase inhibitors.
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- - Levels of circulating calprotectin are higher in primary antiphospholipid syndrome (APS) patients compared to healthy controls, indicating its potential role in the condition.
- - The study revealed calprotectin's association with increased neutrophil counts and C-reactive protein levels, while showing a negative correlation with platelet counts, suggesting its involvement in thrombocytopenia.
- - Mechanistic insights suggested that calprotectin may trigger aPL-mediated thrombocytopenia by activating platelet surface receptors and the NLRP3-inflammasome, leading to reduced platelet viability.