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Review
. 2022 Nov 17:13:1054753.
doi: 10.3389/fimmu.2022.1054753. eCollection 2022.

Neutrophil extracellular traps and complications of liver transplantation

Affiliations
Review

Neutrophil extracellular traps and complications of liver transplantation

Yanyao Liu et al. Front Immunol. .

Abstract

Many end-stage liver disease etiologies are attributed to robust inflammatory cell recruitment. Neutrophils play an important role in inflammatory infiltration and neutrophil phagocytosis, oxidative burst, and degranulation. It has also been suggested that neutrophils may release neutrophil extracellular traps (NETs) to kill pathogens. It has been proven that neutrophil infiltration within the liver contributes to an inflammatory microenvironment and immune cell activation. Growing evidence implies that NETs are involved in the progression of numerous complications of liver transplantation, including ischemia-reperfusion injury, acute rejection, thrombosis, and hepatocellular carcinoma recurrence. NETs are discussed in this comprehensive review, focusing on their effects on liver transplantation complications. Furthermore, we discuss NETs as potential targets for liver transplantation therapy.

Keywords: acute rejection; hepatocellular carcinoma recurrence; ischemia-reperfusion injury; liver transplantation; neutrophil extracellular traps; therapeutic targets; thrombosis.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Mechanisms of NET formation. Three mechanisms of NET formation have been described: lytic NET formation, viable NET formation, and mitochondrial NET formation.
Figure 2
Figure 2
Neutrophil extracellular traps have been implicated in the pathophysiology of several different end-stage liver diseases.
Figure 3
Figure 3
Neutrophil extracellular traps have been implicated in the pathophysiology of liver ischemia-reperfusion injury following liver transplantation. DAMPs, damage-associated molecular patterns; HCQ, Hydroxychloroquine; TMP; Tetramethylpyrazine, rTM; recombinant human thrombomodulin.
Figure 4
Figure 4
Neutrophil extracellular traps have been implicated in the pathophysiology of acute rejection following liver transplantation.
Figure 5
Figure 5
Potential therapeutic targets for NETs. (A) Inhibition of NET formation. (B) Degradation and destabilization of already formed NETs.

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