Neutrophil extracellular traps formation may be involved in the association of propranolol with the development of portal vein thrombosis

Xu, Xiangbo; Xu, Shixue; Zhang, Yiyan; Wang, Le; Yan, Chenghui; Xu, Zihua; Zhao, Qingchun; Qi, Xingshun

doi:10.1016/j.thromres.2024.04.030

Thrombosis Research

2024

DOI: 10.1016/j.thromres.2024.04.030

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Neutrophil extracellular traps formation may be involved in the association of propranolol with the development of portal vein thrombosis

Xiangbo Xu,

Shixue Xu,

Yiyan Zhang

et al.

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Cited by 2 publications

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The Molecular Mechanisms of Portal Vein Thrombosis in Hepatocellular Carcinoma

Galasso,

Cerrito,

Termite

et al. 2024

Cancers

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Hepatocellular carcinoma (HCC) represents the sixth most diagnosed cancer worldwide and is the second leading cause of cancer-related death in the world. The association of HCC and portal vein thrombosis (PVT) represents an advanced stage of the tumor. PVT has a prevalence of about 25–50% in HCC, determining poor prognosis and a remarkable reduction in therapeutic perspectives in these patients, leading to severe complications such as ascites, metastasis, an increase in portal hypertension and potentially fatal gastrointestinal bleeding. The aim of this review is to evaluate the molecular mechanisms that are at the basis of PVT development, trying to evaluate possible strategies in the early detection of patients at high risk of PVT.

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The Molecular Mechanisms of Portal Vein Thrombosis in Hepatocellular Carcinoma

Galasso,

Cerrito,

Termite

et al. 2024

Cancers

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GSDMD-Dependent Neutrophil Extracellular Traps Mediate Portal Vein Thrombosis and Associated Fibrosis in Cirrhosis

Che,

Chien,

Zhu

et al. 2024

IJMS

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Portal vein thrombosis (PVT) is a challenging and controversial complication of cirrhosis. Experimental models that reproduce cirrhotic PVT and effective pharmacological therapies are limited. We aimed to investigate the nature course and mechanisms of PVT in cirrhosis. A novel PVT model was developed via two-step total portal vein ligation in healthy and thioacetamide (TAA)-cirrhotic rats. Circulating and liver-infiltrating neutrophils were isolated from individuals with cirrhosis to examine neutrophil extracellular traps (NETs) and explore their unique characteristics and implications in PVT-associated fibrosis in cirrhosis. We further validated macrophage–myofibroblast transition (MMT) via multiplex immunofluorescence and single-cell sequencing. In the experimental model, cirrhosis promoted PVT development and portal vein intimal thickening. Interestingly, cirrhosis promoted spontaneous resolution of PVT due to instability of thrombus structure, along with pulmonary and intrahepatic clots. NETs-MMT mediate cirrhotic PVT and PVT-associated fibrosis, including fibrotic thrombus remodeling and increased hepatic collagen deposition. Mechanistically, caspase-4-dependent activation of neutrophils and GSDMD mediated the formation of NETs. The extracellular DNA of NETs promoted TGF-β1/Smad3-driven MMT. Inhibiting GSDMD with disulfiram suppressed cirrhotic PVT and prevented associated fibrosis. The cirrhotic PVT model reflected the following three main characteristics of cirrhotic PVT: spontaneous resolution, immunothrombosis, and intimal fibrosis. Targeting NETs with GSDMD inhibitors may serve as a new therapeutic concept to treat cirrhotic PVT.

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Neutrophil extracellular traps formation may be involved in the association of propranolol with the development of portal vein thrombosis

Cited by 2 publications

References 62 publications

The Molecular Mechanisms of Portal Vein Thrombosis in Hepatocellular Carcinoma

The Molecular Mechanisms of Portal Vein Thrombosis in Hepatocellular Carcinoma

GSDMD-Dependent Neutrophil Extracellular Traps Mediate Portal Vein Thrombosis and Associated Fibrosis in Cirrhosis

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