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Von Willebrand factor exacerbates heart failure through formation of neutrophil extracellular traps.
Eur Heart J
October 2024
Department of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China.
Background And Aims: Heart failure (HF) is a leading cause of mortality worldwide and characterized by significant co-morbidities and dismal prognosis. Neutrophil extracellular traps (NETs) aggravate inflammation in various cardiovascular diseases; however, their function and mechanism of action in HF pathogenesis remain underexplored. This study aimed to investigate the involvement of a novel VWF-SLC44A2-NET axis in HF progression.
View Article and Find Full Text PDFInvolvement of peptidylarginine deiminase 4 in eosinophil extracellular trap formation and contribution to citrullinated histone signal in thrombi.
J Thromb Haemost
June 2024
Department of Cardiology and Angiology I, University Heart Center Freiburg-Bad Krozingen, Faculty of Medicine, University of Freiburg, Freiburg, Germany; Department of Cardiology, University Hospital Basel, University of Basel, Basel, Switzerland. Electronic address:
Background: Extracellular traps formed by neutrophils (NETs) and eosinophils (EETs) have been described in coronary thrombi, contributing to thrombus stability. A key mechanism during NET formation is histone modification by the enzyme PAD4. Citrullinated histones, the product of PAD4 activity, are often attributed to neutrophils.
View Article and Find Full Text PDFTo Gain Insights into the Pathophysiological Mechanisms of the Thrombo-Inflammatory Process in the Atherosclerotic Plaque.
Int J Mol Sci
December 2023
Department of Cardiac Surgery, Centre Cardiologique du Nord, 93200 Saint-Denis, France.
Thromboinflammation, the interplay between thrombosis and inflammation, is a significant pathway that drives cardiovascular and autoimmune diseases, as well as COVID-19. SARS-CoV-2 causes inflammation and blood clotting issues. Innate immune cells have emerged as key modulators of this process.
View Article and Find Full Text PDFArabidopsis PHYTOALEXIN DEFICIENT 4 promotes the maturation and nuclear accumulation of immune-related cysteine protease RD19.
J Exp Bot
February 2024
State Key Laboratory Key Laboratory of Ecological Control of Fujian-Taiwan Crop Pests, Plant Immunity Center, Fujian Agriculture and Forestry University, Fuzhou 350002, China.
Arabidopsis PHYTOALEXIN DEFICIENT 4 (PAD4) has an essential role in pathogen resistance as a heterodimer with ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1). Here we investigated an additional PAD4 role in which it associates with and promotes the maturation of the immune-related cysteine protease RESPONSIVE TO DEHYDRATION 19 (RD19). We found that RD19 and its paralog RD19c promoted EDS1- and PAD4-mediated effector-triggered immunity to an avirulent Pseudomonas syringae strain, DC3000, expressing the effector AvrRps4 and basal immunity against the fungal pathogen Golovinomyces cichoracearum.
View Article and Find Full Text PDFPeptidylarginine deiminase 4 and ADAMTS13 activity in bacteraemia.
Philos Trans R Soc Lond B Biol Sci
November 2023
Center for Molecular and Vascular Biology, Department of Cardiovascular Sciences, Immunology and Transplantation, KU Leuven, Leuven, 3000, Belgium.
infection is associated with increased levels of neutrophil extracellular traps (NETs) and von Willebrand factor (VWF), and with reduced activity of ADAMTS13 (a disintegrin and metalloproteinase with thrombospondin type 1 motifs, member 13). Peptidylarginine deiminase 4 (PAD4) contributes to NET formation and inactivates ADAMTS13 . The role of PADs in the dynamics of NETs, VWF and ADAMTS13 has not yet been studied.
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