Endothelin 1 and transforming growth factor-β1 correlate with liver function and portal pressure in cirrhotic patients

Wereszczynka-Siemiatkowska, Urszula; Świdnicka-Siergiejko, Agnieszka Katarzyna; Siemiątkowski, Andrzej; Bondyra, Zofia; Wasielica-Berger, Justyna; Mroczko, Barbara; Janica, Jerzy; Dâbrowski, A

doi:10.1016/j.cyto.2015.05.025

Cited by 11 publications

(8 citation statements)

References 39 publications

(62 reference statements)

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“…In a cirrhotic liver, increased levels of ET-1 and decreased levels of NO contribute to the contraction of hepatic stellate cells [ 38 ]. Wereszczynka-Siemiatkowska et al showed that peripheral ET-1 levels reflect the stage of PH and liver insufficiency in cirrhosis [ 39 ] and are correlated significantly with liver laboratory parameters and HVPG. In our study, we found that after TIPS placement and OCT-LAR treatment, a slight decrease in ET-1 and an increase in NO x levels in hepatic venous blood were observed during follow-up period but without difference.…”

Section: Discussionmentioning

confidence: 99%

Effects of a Long-Acting Formulation of Octreotide on Patients with Portal Hypertension

Cui

Yao

Zhu

et al. 2017

Gastroenterology Research and Practice

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Objective This study aimed to determine whether the treatment of a long-acting formulation of octreotide (OCT-LAR) exerted a similar effect on improving the prognosis of patients with portal hypertension compared with placement of transjugular intrahepatic portosystemic shunts (TIPSs). Methods A total of 24 patients with portal hypertension who underwent TIPS placement or OCT-LAR treatment from January 2010 to January 2015 were reviewed. Hemodynamic studies, biological values, live functions, and treatment complications before and during the treatment were evaluated. Results Baseline clinical characteristics were similar between two groups. Hepatic venous pressure gradient (HVPG) was improved in OCT-LAR groups (15.9 ± 2.4 to 12.8 ± 1.6 mmHg). Both groups showed a slight decrease in endothelin-1 (ET-1) and urotensin II and a slight increase in oxide metabolite (NOx) concentrations with no significant difference. Aspartate aminotransferase and alanine aminotransferase increased one week after TIPS placement when they improved in the OCT-LAR treatment group. The complications of OCT-LAR treatment were minor and transient. However, one patient who received TIPS placement presented procedure-related complications and required rehospitalization, and 2 patients had developed hepatic encephalopathy during the follow-up period. Conclusion Prolonged administration of OCT-LAR exerted a virtually similar effect on improving hemodynamic parameters and liver function in patients with portal hypertension compared with placement of TIPS, with no apparent serious adverse effects.

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Section: Discussionmentioning

confidence: 99%

Effects of a Long-Acting Formulation of Octreotide on Patients with Portal Hypertension

Cui

Yao

Zhu

et al. 2017

Gastroenterology Research and Practice

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“…ET-1 may play an important role in liver disease, especially in circulatory disorders such as portal hypertension and ischemia. ET-1 acts as a paracrine hormone and its plasma levels could represent an overflow of locally produced peptides [ 15 ]. Fluid shear stress is a strong liberator of ET-1 from splanchnic vascular endothelial cells, and TIPS could markedly reduce the PVPG and fluid shear stress [ 16 ].…”

Section: Discussionmentioning

confidence: 99%

Systemic and Splanchnic Lipopolysaccharide and Endothelin-1 Plasma Levels in Liver Cirrhosis before and after Transjugular Intrahepatic Portosystemic Shunt

Meng

Wang

et al. 2016

Gastroenterology Research and Practice

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Lipopolysaccharide (LPS) and endothelin- (ET-) 1 may aggravate portal hypertension by increasing intrahepatic resistance and splanchnic blood flow. In the portal vein, after TIPS shunting, LPS and ET-1 were significantly decreased. Our study suggests that TIPS can benefit cirrhotic patients not only in high hemodynamics related variceal bleeding but also in intestinal bacterial translocation associated complications such as endotoxemia.

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“…22 Increased plasma ET-1 and ET-3 levels were observed in patients with CLD and portal hypertension. [26][27][28] The role of ET-2 is not reported in CLD conditions. In liver microenvironment, ET-1 synthesized by LSECs acts on several cell types nearby such as hepatocytes, HSCs, and Kupffer cells via paracrine fashion.…”

Section: Endothelin-1: Synthesis Receptors and Functionmentioning

confidence: 99%

Endothelin-1 in portal hypertension: The intricate role of hepatic stellate cells

Ezhilarasan

2020

Exp Biol Med (Maywood)

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Portal hypertension is one of the most important cirrhosis-associated complications of chronic liver disease, leading to significant morbidity and mortality. After chronic liver injury, hepatic stellate cells reside in the perisinusoidal space activted and acquire a myofibroblast-like phenotype. The activated hepatic stellate cells act as both sources as well as the target for a potent vasoconstrictor endothelin-1. Activation of hepatic stellate cells plays a vital role in the onset of cirrhosis by way of increased extracellular matrix production and the enhanced contractile response to vasoactive mediators such as endothelin-1. In fibrotic/cirrhotic liver, activated hepatic stellate cells produce endothelin-1 leading to an imbalance between pro and antifibrotic factors responsible for enormous extracellular matrix synthesis. Thus, extracellular matrix deposition in the perisinusoidal space further augments liver stiffness and elevates the vascular tone and portal hypertension. Portal hypertension is a complex process modulated by several cell types like hepatic stellate cells, liver sinusoidal endothelial cells, Kupffer cells, injured hepatocytes, immune cells, and biliary epithelial cells. Therefore, targeting a single cell type may not be useful for regression of cirrhosis and portal hypertension. Nevertheless, numerous findings indicate that functionally liver sinusoidal endothelial cells and hepatic stellate cells closely regulate the sinusoidal blood flow via synthesis of several vasoactive molecules including endothelin-1, and hence targeting these cells with novel pharmacological agents may offer promising results. Impact statement Portal hypertension is pathologically defined as increase of portal venous pressure, mainly due to chronic liver diseases such as fibrosis and cirrhosis. In fibrotic liver, activated hepatic stellate cells increase their contraction in response to endothelin-1 (ET-1) via autocrine and paracrine stimulation from liver sinusoidal endothelial cells and injured hepatocytes. Clinical studies are limited with ET receptor antagonists in cirrhotic patients with portal hypertension. Hence, studies are needed to find molecules that block ET-1 synthesis. Accumulation of extracellular matrix proteins in the perisinusoidal space, tissue contraction, and alteration in blood flow are prominent during portal hypertension. Therefore, novel matrix modulators should be tested experimentally as well as in clinical studies. Specifically, tumor necrosis factor-α, transforming growth factor-β1, Wnt, Notch, rho-associated protein kinase 1 signaling antagonists, and peroxisome proliferator-activated receptor α and γ, interferon-γ and sirtuin 1 agonists should be tested elaborately against cirrhosis patients with portal hypertension.

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Endothelin 1 and transforming growth factor-β1 correlate with liver function and portal pressure in cirrhotic patients

Cited by 11 publications

References 39 publications

Effects of a Long-Acting Formulation of Octreotide on Patients with Portal Hypertension

Effects of a Long-Acting Formulation of Octreotide on Patients with Portal Hypertension

Systemic and Splanchnic Lipopolysaccharide and Endothelin-1 Plasma Levels in Liver Cirrhosis before and after Transjugular Intrahepatic Portosystemic Shunt

Endothelin-1 in portal hypertension: The intricate role of hepatic stellate cells

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