Evaluation of Plasma Urokinase-Type Plasminogen Activator Receptor (UPAR) in Patients With Chronic Hepatitis B, C and Non-Alcoholic Fatty Liver Disease (NAFLD) as Serological Fibrosis Marker

Akdoğan, Özlem; Yücel, Ayşegül Atak; Sargın, Zeynep Gök; Sönmez, Cemile; Yılmaz, Güldal; Özeni̇rler, Seren

doi:10.1016/j.jceh.2018.02.001

Cited by 8 publications

(5 citation statements)

References 33 publications

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“…The current study showed a significant increase in sUPAR among HCV patients with hepatic fibrosis as compared with controls. This was in agreement with Akdogan et al, who reported that sUPAR was higher in chronic HCV patients with hepatic fibrosis as compared with controls [15].…”

Section: Discussionsupporting

confidence: 93%

Evaluation of Plasma Urokinase-Type Plasminogen Activator Receptor and Interleukin 34 in Patients with Chronic Hepatitis C as Serological Fibrosis Markers

Abdulwehab¹,

Ahmed²,

El-Zefzafy³

et al. 2021

OJI

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Background: Hepatitis C Virus (HCV) infection is a progressive disease that may result in chronic hepatitis, fibrosis and cirrhosis. Assessment of liver fibrosis is an essential factor in the management of chronic HCV. Objective: To evaluate plasma soluble Urokinase Plasminogen Activator Receptor (sU-PAR) and interleukin-34 (IL-34) as serological markers of liver fibrosis in patients with chronic HCV. Methods: This case-control study enrolled 60 chronic HCV patients who were subdivided into three groups of mild, moderate and severe hepatic fibrosis depending on Fibrosis-4 score (FIB-4). Patients were compared with 20 age and sex-matched controls. Plasma sUPAR and IL-34 levels were measured by Enzyme Linked Immunosorbent Assay (ELISA). Results: Plasma sUPAR and IL-34 were significantly increased in HCV patients when compared with controls, and their increase was positively correlated with the progression of hepatic fibrosis. Plasma sUPAR and IL-34 positively correlated with Aspartate Aminotransferase (AST) and Alanine Aminotransferase (ALT), and negatively correlated with hemoglobin concentration and platelet count. The output data of Receiver Operating Characteristic (ROC) curve to differentiate patients from controls revealed that sU-PAR at cut-off > 186.2 ng/L and Area Under Curve (AUC) of 0.944 had (85%) sensitivity and (100%) specificity, and IL-34 at cut off > 16.4 ng/L and AUC of 0.942 had (75%) sensitivity and (100%) specificity. The output data of ROC curve to differentiate severe from mild to moderate hepatic fibrosis patients revealed that sUPAR at cut-off > 510 ng/L and AUC of 0.

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Section: Discussionsupporting

confidence: 93%

Evaluation of Plasma Urokinase-Type Plasminogen Activator Receptor and Interleukin 34 in Patients with Chronic Hepatitis C as Serological Fibrosis Markers

Abdulwehab¹,

Ahmed²,

El-Zefzafy³

et al. 2021

OJI

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“…There is a link between expression levels of uPA/uPAR and the severity of liver fibrosis in patients. The uPAR may serve as a biomarker for both the presence and the severity of liver fibrosis (Akdogan et al, ; Sjowall, Martinsson, Cardell, Ekstedt, & Kechagias, ; Zimmermann, Koch, Seidler, Trautwein, & Tacke, ). However, uPA may not directly degrade the fibrillar collagens (Carmeliet et al, ).…”

Section: Discussionmentioning

confidence: 99%

Curcumol may reverse early and advanced liver fibrogenesis through downregulating the uPA/uPAR pathway

Lin

Peng

et al. 2020

Phytotherapy Research

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Previous studies have suggested strong antifibrotic activity of curcumol in the liver; the underlying mechanisms of which, however, remain largely unknown. Aiming to investigate the role of curcumol in regulating early and advanced liver fibrosis, we designed a rat model with advanced liver fibrosis and cell model with an initial fibrotic stage. Model rats induced by CCl 4 and alcohol presented advanced liver fibrosis with complete fibrous septa. The administration of curcumol (25 mg/kg or 50 mg/kg) resulted in reversal of liver fibrosis. Leptin-administrated liver sinusoidal endothelial cells presented defenestration and basement membrane components deposition, including laminin (LN) and type IV collagen (Col IV), the characteristics of capillarization by scanning electron microscopy and immunofluorescence assays. After treatment with curcumol (12.5, 25, or 50 mg/L), defenestration was restored and the levels of LN and Col IV were decreased, consistent with the rat model. Quantitative polymerase chain reaction and Western blot results revealed that increased levels of urokinase plasminogen activator (uPA)/ uPA receptor (uPAR) were observed both in vivo and in vitro, curcumol significantly reduced uPA/uPAR at both the mRNA and protein levels. Reduction of uPA/uPAR may be synergistic with matrix metallopeptidase 13 to reverse liver fibrogenesis. In conclusion, curcumol protects liver from phenotypic changes in the early and advanced fibrogenesis, possibly through uPA/uPAR pathway.

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“…uPAR is expressed on a variety of cells, including fibroblasts, monocytes, macrophages, keratinocytes, neurons, ECs and smooth muscle cells [ 27 ], and uPAR expression is induced by inflammation [ 33 , 55 ]. It has been reported that increased uPAR expression is observed in many fibrosis-related diseases, including cardiac fibrosis, idiopathic pulmonary fibrosis, and SSc ( Figure 5 ) [ 56 , 57 , 58 , 59 , 60 , 61 , 62 , 63 ].…”

Section: The Upa and Upar Systemmentioning

confidence: 99%

The uPA/uPAR System Orchestrates the Inflammatory Response, Vascular Homeostasis, and Immune System in Fibrosis Progression

Kanno

2023

IJMS

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Fibrotic diseases, such as systemic sclerosis (SSc), idiopathic pulmonary fibrosis, renal fibrosis and liver cirrhosis are characterized by tissue overgrowth due to excessive extracellular matrix (ECM) deposition. Fibrosis progression is caused by ECM overproduction and the inhibition of ECM degradation due to several events, including inflammation, vascular endothelial dysfunction, and immune abnormalities. Recently, it has been reported that urokinase plasminogen activator (uPA) and its receptor (uPAR), known to be fibrinolytic factors, orchestrate the inflammatory response, vascular homeostasis, and immune homeostasis system. The uPA/uPAR system may show promise as a potential therapeutic target for fibrotic diseases. This review considers the role of the uPA/uPAR system in the progression of fibrotic diseases.

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Evaluation of Plasma Urokinase-Type Plasminogen Activator Receptor (UPAR) in Patients With Chronic Hepatitis B, C and Non-Alcoholic Fatty Liver Disease (NAFLD) as Serological Fibrosis Marker

Cited by 8 publications

References 33 publications

Evaluation of Plasma Urokinase-Type Plasminogen Activator Receptor and Interleukin 34 in Patients with Chronic Hepatitis C as Serological Fibrosis Markers

Evaluation of Plasma Urokinase-Type Plasminogen Activator Receptor and Interleukin 34 in Patients with Chronic Hepatitis C as Serological Fibrosis Markers

Curcumol may reverse early and advanced liver fibrogenesis through downregulating the uPA/uPAR pathway

The uPA/uPAR System Orchestrates the Inflammatory Response, Vascular Homeostasis, and Immune System in Fibrosis Progression

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