Cytomegalovirus Latency Exacerbated Small-for-size Liver Graft Injury Through Activation of CCL19/CCR7 in Hepatic Stellate Cells

Liu, Xiao Bing; Liu, Hui; Liu, Jiang; Cheung, Allen Ka Loon; Zheng, Ming; Cheng, Jin Lin; Liu, Qing Sheng; Lo, Chung Mau; Chen, Zhiwei; Man, Kwan

doi:10.1097/tp.0000000000003846

Cited by 3 publications

(1 citation statement)

References 41 publications

(68 reference statements)

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“…In addition, many other chemokines and their receptors are involved in the pathogenesis of liver fibrosis, including C-X-C motif ligand 12 (CXCL12) /C-X-C receptor 4[ 52 ], chemokine (C-X3-C motif) ligand 1/C-X3-C receptor 1 (CX3CR1)[ 53 ], CCL19/CCR7[ 54 ], and CXCL12/atypical chemokine receptor 3[ 55 ].…”

Section: Signaling Pathways and Molecular Targets For Liver Fibrosis ...mentioning

confidence: 99%

Treatment of liver fibrosis: Past, current, and future

Zhang¹,

Liu²,

Yang³

2023

World J Hepatol

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Liver fibrosis accompanies the progression of chronic liver diseases independent of etiologies, such as hepatitis viral infection, alcohol consumption, and metabolic-associated fatty liver disease. It is commonly associated with liver injury, inflammation, and cell death. Liver fibrosis is characterized by abnormal accumulation of extracellular matrix components that are expressed by liver myofibroblasts such as collagens and alpha-smooth actin proteins. Activated hepatic stellate cells contribute to the major population of myofibroblasts. Many treatments for liver fibrosis have been investigated in clinical trials, including dietary supplementation ( e.g. , vitamin C), biological treatment ( e.g. , simtuzumab), drug ( e.g. , pegbelfermin and natural herbs), genetic regulation ( e.g. , non-coding RNAs), and transplantation of stem cells ( e.g. , hematopoietic stem cells). However, none of these treatments has been approved by Food and Drug Administration. The treatment efficacy can be evaluated by histological staining methods, imaging methods, and serum biomarkers, as well as fibrosis scoring systems, such as fibrosis-4 index, aspartate aminotransferase to platelet ratio, and non-alcoholic fatty liver disease fibrosis score. Furthermore, the reverse of liver fibrosis is slowly and frequently impossible for advanced fibrosis or cirrhosis. To avoid the life-threatening stage of liver fibrosis, anti-fibrotic treatments, especially for combined behavior prevention, biological treatment, drugs or herb medicines, and dietary regulation are needed. This review summarizes the past studies and current and future treatments for liver fibrosis.

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Section: Signaling Pathways and Molecular Targets For Liver Fibrosis ...mentioning

confidence: 99%

Treatment of liver fibrosis: Past, current, and future

Zhang¹,

Liu²,

Yang³

2023

World J Hepatol

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CC chemokines family in fibrosis and aging: From mechanisms to therapy

Lei

Jia

Wang

et al. 2023

Ageing Research Reviews

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New Insights in Mechanisms and Therapeutics for Short- and Long-Term Impacts of Hepatic Ischemia Reperfusion Injury Post Liver Transplantation

Liu

Man

2021

IJMS

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Liver transplantation has been identified as the most effective treatment for patients with end-stage liver diseases. However, hepatic ischemia reperfusion injury (IRI) is associated with poor graft function and poses a risk of adverse clinical outcomes post transplantation. Cell death, including apoptosis, necrosis, ferroptosis and pyroptosis, is induced during the acute phase of liver IRI. The release of danger-associated molecular patterns (DAPMs) and mitochondrial dysfunction resulting from the disturbance of metabolic homeostasis initiates graft inflammation. The inflammation in the short term exacerbates hepatic damage, leading to graft dysfunction and a higher incidence of acute rejection. The subsequent changes in the graft immune environment due to hepatic IRI may result in chronic rejection, cancer recurrence and fibrogenesis in the long term. In this review, we mainly focus on new mechanisms of inflammation initiated by immune activation related to metabolic alteration in the short term during liver IRI. The latest mechanisms of cancer recurrence and fibrogenesis due to the long-term impact of inflammation in hepatic IRI is also discussed. Furthermore, the development of therapeutic strategies, including ischemia preconditioning, pharmacological inhibitors and machine perfusion, for both attenuating acute inflammatory injury and preventing late-phase disease recurrence, will be summarized in the context of clinical, translational and basic research.

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Cytomegalovirus Latency Exacerbated Small-for-size Liver Graft Injury Through Activation of CCL19/CCR7 in Hepatic Stellate Cells

Cited by 3 publications

References 41 publications

Treatment of liver fibrosis: Past, current, and future

Treatment of liver fibrosis: Past, current, and future

CC chemokines family in fibrosis and aging: From mechanisms to therapy

New Insights in Mechanisms and Therapeutics for Short- and Long-Term Impacts of Hepatic Ischemia Reperfusion Injury Post Liver Transplantation

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