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. 2021 Oct 22;12(11):984. doi: 10.1038/s41419-021-04294-3

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© The Author(s) 2021

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — A In diabetic mouse wounds, NET formation is increased, and inflammation is sustained by the NLRP3 inflammasome-NET loop due to macrophage activation and MFG-E8 deficiency. Increased LRG1 in hyperglycemic mouse blood has been shown to upregulate NET formation via the Akt pathway. PKC βII exhibits hyperactivity in diabetes and contributes to excess NET formation. In addition, GnRH expressed on neutrophils enhances NET formation in the wound area. B In normoglycemic wounds, dectin-2 increases the neutrophil inflammatory response and NET formation. Neutrophil-derived FXII modulates neutrophil NET formation by upregulating αMβ2 integrin and increasing intracellular calcium.