The emerging roles of neutrophil extracellular traps in wound healing

Shuainan Zhu,Xiaomin Ling,Changhong Miao,Liying Xu,Ying Yu,Yan Hu,Yun Ren,Kefang Guo,Huilin Wang,Hao Zhang,Lin Jin

doi:10.1038/s41419-021-04294-3

Abstract

Delayed wound healing causes problems for many patients both physically and psychologically, contributing to pain, economic burden, loss of function, and even amputation. Although many factors affect the wound healing process, abnormally prolonged or augmented inflammation in the wound site is a common cause of poor wound healing. Excessive neutrophil extracellular trap (NET) formation during this phase may amplify inflammation and hinder wound healing. However, the roles of NETs in wound healing are still unclear. Herein, we briefly introduce NET formation and discuss the possible NET-related mechanisms in wound healing. We conclude with a discussion of current studies, focusing on the roles of NETs in diabetic and normoglycemic wounds and the effectiveness of NET-targeting treatments in wound healing.

Highlights

Wound healing is a delicate biological process that includes four overlapping phases, and disruption of any phase can result in delayed healing or lack of healing [1]
Circulating neutrophils are among the first cells to be recruited to the wound site; [5] these cells function through phagocytosis, degranulation, and the release of neutrophil extracellular traps (NETs)
The gonadotropin-releasing hormone (GnRH) receptor, which is expressed on the surfaces of neutrophils, participates in diabetic wound healing, and GnRH-enhanced neutrophils undergoing phorbol myristate acetate (PMA)-induced NET formation contribute to wound impairment [89]

Summary

Introduction

Wound healing is a delicate biological process that includes four overlapping phases (rapid hemostasis, appropriate inflammation, proliferation, and remodeling), and disruption of any phase can result in delayed healing or lack of healing [1]. These researchers Increased NET formation after PAD4 overexpression has been proposed that the migration of keratinocytes was probably found to lead to poor vascularization and vascular remodeling in inhibited by NETs and resulted in delayed wound healing, but a model of stroke, and anti-NET treatments such as DNase1 or further investigation is needed to verify this conclusion [7].

Results

Conclusion