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- Aldo Bonaventura
- Pauley Heart Center, Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University, 1200 E Marshall St, Richmond, VA 23298, USA
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- Alessandra Vecchié
- Pauley Heart Center, Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University, 1200 E Marshall St, Richmond, VA 23298, USA
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- Antonio Abbate
- Pauley Heart Center, Division of Cardiology, Department of Internal Medicine, Virginia Commonwealth University, 1200 E Marshall St, Richmond, VA 23298, USA
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- Fabrizio Montecucco
- First Clinic of Internal Medicine, Department of Internal Medicine and Centre of Excellence for Biomedical Research (CEBR), University of Genoa, viale Benedetto XV 6, 16132 Genoa, Italy
説明
<jats:p>Neutrophil extracellular traps (NETs) are formed by decondensed chromatin, histones, and neutrophil granular proteins and have a role in entrapping microbial pathogens. NETs, however, have pro-thrombotic properties by stimulating fibrin deposition, and increased NET levels correlate with larger infarct size and predict major adverse cardiovascular (CV) events. NETs have been involved also in the pathogenesis of diabetes, as high glucose levels were found to induce NETosis. Accordingly, NETs have been described as drivers of diabetic complications, such as diabetic wound and diabetic retinopathy. Inflammasomes are macromolecular structures involved in the release of pro-inflammatory mediators, such as interleukin-1, which is a key mediator in CV diseases. A crosstalk between the inflammasome and NETs is known for some rheumatologic diseases, while this link is still under investigation and not completely understood in CV diseases. In this review, we summarized the most recent updates about the role of NETs in acute myocardial infarction and metabolic diseases and provided an overview on the relationship between NET and inflammasome activities in rheumatologic diseases, speculating a possible link between these two entities also in CV diseases.</jats:p>
収録刊行物
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- Cells
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Cells 9 (1), 231-, 2020-01-17
MDPI AG