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Neutrophil extracellular traps (NETs) are implicated in thrombosis and inflammation during acute myocardial infarction (AMI), but their kinetics, local distribution, and clinical relevance remain unclear. We conducted a prospective study in 144 patients with ST-segment elevation (STEMI) and non-ST-segment elevation AMI (NSTEMI) undergoing coronary angioplasty (PCI), quantifying double-stranded DNA (dsDNA), myeloperoxidase (MPO), and neutrophil elastase (NE) in the infarct-related artery (IRA), contralateral coronary artery (CCA), and peripheral blood. Coronary thrombi and DNASE1 Q222R were also analysed. NET markers were elevated in the IRA, and NE and dsDNA increased peripherally after PCI. IRA NE levels independently predicted cardiovascular events (HR, 1.76; 95%CI: 1.24 - 2.51). Thrombi with higher NE and citrullinated histone H3 content were associated with suboptimal PCI results. dsDNA levels were significantly higher in patients with the GG DNASE1 genotype. These findings indicate a compartmentalized NET response in AMI and support a potential prognostic impact of NETs.
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http://dx.doi.org/10.1007/s12265-025-10676-1 | DOI Listing |
Toxicol Sci
September 2025
Department of Pharmacology, Rutgers University Robert Wood Johnson Medical School, Piscataway, NJ, USA.
Neutrophils play a complex role in the pathogenesis of chronic liver disease and have been linked to both liver damage and injury resolution. Recent reports propose that neutrophils drive liver injury and fibrosis through the formation of neutrophil extracellular traps (NETs). This study tests the hypothesis that the enzyme peptidyl arginine deiminase-4 (PAD4) drives NET formation and liver fibrosis in experimental chronic liver injury.
View Article and Find Full Text PDFBackground: The goal was to explore the impact of the NR1D1 gene on the occurrence, development, and prognosis of colorectal cancer (CRC) using bioinformatics approaches.
Methods: CRC transcriptomic and clinical data from TCGA were analyzed to compare NR1D1 expression in tumors and various clinical stages. Survival differences between high and low NR1D1 expression groups were assessed using the R survival package.
FASEB J
September 2025
National Heart Center Singapore, Singapore, Singapore.
Cardiovascular diseases are increasingly recognized as chronic disorders driven by a complex interplay between inflammation and fibrosis. In this review, we elucidate emerging mechanisms that govern the transition from acute inflammation to pathological fibrosis, with particular focus on cellular crosstalk between neutrophils, macrophages, fibroblasts, and myofibroblasts. We explore how dysregulated immune responses and extracellular matrix (ECM) remodeling sustain a pathogenic feedback loop, promoting myocardial stiffening and adverse cardiac remodeling.
View Article and Find Full Text PDFImmunology
September 2025
Department of Biochemical Science and Technology, National Taiwan University, Taipei, Taiwan, ROC.
Enolase-1 (ENO1) is a moonlighting protein with multiple functions. When expressed on the cell surface, ENO1 binds plasminogen (PLG) and promotes cell migration by facilitating plasmin (PLM)-mediated extracellular matrix degradation. Here, we observed that inflammatory stimulation significantly upregulated ENO1 expression on the neutrophil surface, both in vitro and in vivo.
View Article and Find Full Text PDFSci Rep
September 2025
Shanghai Key Laboratory of Molecular Imaging, Shanghai University of Medicine and Health Science, 279Th Zhouzhu Road, Shanghai, 201318, China.