Overexpression of apelin receptor (APJ/AGTRL1) on hepatic stellate cells and sinusoidal angiogenesis in human cirrhotic liver

Yokomori, Hiroaki; Oda, Masaya; Yoshimura, Kazunori; Machida, Sanae; Kaneko, Fumihiko; Hibi, Toshifumi

doi:10.1007/s00535-010-0296-3

Cited by 31 publications

(41 citation statements)

References 25 publications

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“…In addition, apelin contributes to platelet-derived growth factor-induced proliferation of HSC's in vitro [12], all of which are known to contribute largely to fibrosis progression and extracellular matrix deposition [30, 31]. In this setting, we also found apelin serum level to be significantly elevated in patients with fibrosis.…”

Section: Discussionsupporting

confidence: 57%

Apelin Serum Level in Egyptian Patients with Chronic Hepatitis C

El‐Mesallamy

Hamdy

Rizk

et al. 2011

Mediators of Inflammation

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Objective. Highlighting the apelin system would present a new therapeutic target for liver disease. Apelin; endogenous ligand for the orphan receptor APJ, was recently suggested to be associated with fibrosis progression and cirrhosis in addition to insulin resistance (IR) and inflammation. The present study was conducted to evaluate blood apelin level changes among 73 chronic hepatitis C (CHC) Egyptian patients and if associated with body mass index (BMI), IR, and tumor necrosis factor-alpha (TNF-α). Serum apelin levels were significantly higher in patients with CHC with median value (3.25) when compared with controls (1.11), at P < 0.0001, with significant apelin variations among asymptomatic carriers (ASC), fibrosis, and cirrhosis patients, and also among obese and nonobese patients. Multiple regression analysis depicted that BMI, triglycerides, and total cholesterol were independent correlation factors to apelin levels, whereas TNF-α was found to be significantly negatively correlated to adjusted apelin in CHC patients (r = −0.5944, P < 0.0001). IR was positively correlated to adjusted apelin in CHC patients (r = 0.2663, P < 0.05). Conclusion. Apelin level varies among stages of CHC, which may contribute to fibrosis progression. In addition, obesity and IR could act as comorbid factors affecting apelin level in patients with CHC.

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Section: Discussionsupporting

confidence: 57%

Apelin Serum Level in Egyptian Patients with Chronic Hepatitis C

El‐Mesallamy

Hamdy

Rizk

et al. 2011

Mediators of Inflammation

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“…Previous studies have demonstrated that apelin/APJ axis is one of the important signalling pathways involved in the pathological fibrotic processes, such as liver cirrhosis. Apelin and its receptor APJ are expressed at high levels in hepatic stellate cells (HSC) of human cirrhotic liver 10,18 . Pro‐fibrotic factors, such as angiotensin II and endothelin‐1, increase the expression of apelin in human LX‐2 HSC line, 10 whereas hypoxia and lipopolysaccaride stimulate the expression of APJ in those cells 19 .…”

Section: Discussionmentioning

confidence: 99%

Serum apelin levels: clinical association with vascular involvements in patients with systemic sclerosis

Aozasa

Asano

Akamata

et al. 2011

Acad Dermatol Venereol

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“…It has been found that APJ was expressed in Kupffer cells, and it inhibited liver regeneration after partial hepatectomy in mice (Yoshiya et al, 2015). In addition, the apelin/APJ was expressed in human hepatic stellate cells (HSCs), and promoted liver fibrosis or cirrhosis progression (Melgar-Lesmes et al, 2010; Yokomori et al, 2011). …”

Section: Distribution and Expression Of Apelin In Livermentioning

confidence: 99%

“…Melgar-Lesmes et al (2011) reported that apelin expression in HSCs was enhanced under hypoxic or proinflammatory conditions, and apelin could increase the synthesis of platelet-derived growth factor β receptor (PDGF-β) and collagen-I in LX-2 cells. Yokomori et al (2011) reported that, in cultured HSCs, APJ expression was sharply increased by PDGF-β. The function of apelin/APJ in liver fibrosis still needs to be investigated.…”

Section: Function Of the Apelin/apj In Physiology And Pathophysiologymentioning

confidence: 99%

The Role of the Apelin/APJ System in the Regulation of Liver Disease

Kong

Chen

et al. 2017

Front. Pharmacol.

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Apelin is an endogenous peptide that is a ligand for the APJ receptor (angiotensin II receptor like-1, AT-1). The apelin/APJ system is distributed in diverse periphery organ tissues. It has been shown that the apelin/APJ system plays various roles in physiology and pathophysiology of many organs. It regulates cardiovascular development or cardiac disease, glycometabolism and fat metabolism as well as metabolic disease. The apelin/APJ system participates in various cell activities such as proliferation, migration, apoptosis or inflammation. However, apelin/APJ function in the liver is still under investigation. In the liver, the apelin-APJ system could play an inhibitory role in liver regeneration and promote Fas-induced apoptosis. It may participate in the formation of hepatic fibrosis or cirrhosis, and even cancer. In this review, we summarize the role of the apelin/APJ system in liver disease.

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Overexpression of apelin receptor (APJ/AGTRL1) on hepatic stellate cells and sinusoidal angiogenesis in human cirrhotic liver

Abstract: Enhanced expression of APJ on HSCs in cirrhosis indicates markedly increased vascular remodeling.

Cited by 31 publications

References 25 publications

Apelin Serum Level in Egyptian Patients with Chronic Hepatitis C

Apelin Serum Level in Egyptian Patients with Chronic Hepatitis C

Serum apelin levels: clinical association with vascular involvements in patients with systemic sclerosis

The Role of the Apelin/APJ System in the Regulation of Liver Disease

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