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. 2022 Mar 25;23(7):3573. doi: 10.3390/ijms23073573

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© 2022 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).

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Summary of potential roles of neutrophil extracellular traps (NETs) in cancer treatment-related cardiovascular toxicity. Neutrophil extracellular traps (NETs) ^a, bearing DNA strands and released proteins containing myeloperoxidase, Cathepsin G, neutrophil elastase (NE), and proteinase 3 (PR3), a series of phospholipases, hypochlorous acid (HOCl) and pro-IL (interleukin)-1α; NETosis triggers ^b, including activated platelets while in contact with collagen, IL-8, TNF, pathogens, PMA…etc. Possible candidates for mitigating NETs burden to increase cancer survival and reduce cancer treatment-related cardiovascular toxicity (CTRCT) ^c: including (1) Potent anti-platelet therapy, (2) Deoxyribonuclease (DNase I), (3) Inhibition of peptidyl arginine deiminase-4 (PAD-4), (4) Inhibition of myeloperoxidase (MPO), (5) Anti-cytokine therapy (e.g., targeting IL-1 isoforms, IL-8, or IL-6), (6) Inhibition serine proteases.