Role of the receptor for advanced glycation end products inhepatic fbrosis

Lohwasser, Christina; Neureiter, Daniel; Popov, Yury; Bauer, Michael; Schuppan, Detlef

doi:10.3748/wjg.15.5789

Cited by 47 publications

(52 citation statements)

References 51 publications

(67 reference statements)

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“…Our results are also in line with prior findings in CCl4-induced hepatic fibrosis where RAGE transcript and protein levels were upregulated until 6 weeks after the completion of CCl4 treatment [32]. Furthermore, it has been shown that α-SMA-positive HSC/myofibroblasts of the septal or portal interface, representing the prominent fibrogenic effectors, expressed RAGE in both fibrosis models.…”

Section: Discussionsupporting

confidence: 81%

Can Pharmacological Targeting of Advanced Glycation End Products Provide Protection Against Experimentally Induced Liver Fibrosis?

Am¹,

Guemei²

2015

Biochem Pharmacol (Los Angel)

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Section: Discussionsupporting

confidence: 81%

Can Pharmacological Targeting of Advanced Glycation End Products Provide Protection Against Experimentally Induced Liver Fibrosis?

Am¹,

Guemei²

2015

Biochem Pharmacol (Los Angel)

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“…Patients with chronic liver injuries were found to exhibit significantly higher hepatic RAGE expression levels [99] , and in NAFLD patients a correlation was detected between the severity of fibrosis and the patients' serum TAGE concentrations, indicating that RAGE and TAGE make significant contributions to the development of liver disease [23] . In addition, DM, which upregulates AGE synthesis and RAGE expression, has been found to accelerate the progression of fibrosis in a number of human liver conditions, including chronic hepatitis C and NAFLD [100] .…”

Section: The Inhibition Of Tage Synthesis: Acarbosementioning

confidence: 99%

Involvement of the TAGE-RAGE system in non-alcoholic steatohepatitis: Novel treatment strategies

Takeuchi

Takino

Sakasai-Sakai

et al. 2014

WJH

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Non-alcoholic fatty liver disease (NAFLD) is a major cause of liver disease around the world. It includes a spectrum of conditions from simple steatosis to non-alcoholic steatohepatitis (NASH) and can lead to fibrosis, cirrhosis, liver failure, and/or hepatocellular carcinoma. NAFLD is also associated with other medical conditions such as obesity, diabetes mellitus (DM), metabolic syndrome, hypertension, insulin resistance, hyperlipidemia, and cardiovascular disease (CVD). In diabetes, chronic hyperglycemia contributes to the development of both macro-and microvascular conditions through a variety of metabolic pathways. Thus, it can cause a variety of metabolic and hemodynamic conditions, including upregulated advanced glycation end-products (AGEs) synthesis. In our previous study, the most abundant type of toxic AGEs (TAGE); i.e. , glyceraldehyde-derived AGEs, were found to make a significant contribution to the pathogenesis of DM-induced angiopathy. Furthermore, accumulating evidence suggests that the binding of TAGE with their receptor (RAGE) induces oxidative damage, promotes inflammation, and causes changes in intracellular signaling and the expression levels of certain genes in various cell populations including hepatocytes and hepatic stellate cells. All of these effects could facilitate the pathogenesis of hypertension, cancer, diabetic vascular complications, CVD, dementia, and NASH. Thus, inhibiting TAGE synthesis, preventing TAGE from binding to RAGE, and downregulating RAGE expression and/or the expression of associated effector molecules all have potential as therapeutic strategies against NASH. Here, we examine the contributions of RAGE and TAGE to various conditions and novel treatments that target them in order to prevent the development and/or progression of NASH. Key words: Non-alcoholic fatty liver disease; Non-alcoholic steatohepatitis; Advanced glycation end-products; Toxic advanced glycation end-products; Receptor for advanced glycation end-products; Toxic advanced glycation end-products-receptor for advanced glycation end-products system; Diabetes mellitus; Cardiovascular disease; Dietary fructose; Dietary advanced glycation end-products TOPIC HIGHLIGHT

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“…Previous studies have demonstrated that RAGE-specific small interfering (si)RNA is able to inhibit the expression of the RAGE gene in primary rat hepatic stellate cells (HSCs), and may be able to inhibit the generation of profibrogenic cytokines (5)(6)(7). Furthermore, high expression levels of RAGE mRNA and protein have been observed in activated HSCs and CCl 4 -induced HF rats.…”

Section: Introductionmentioning

confidence: 99%

Small interfering RNA targeting receptor for advanced glycation end products suppresses the generation of proinflammatory cytokines

Wang

Xia

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. The aim of the present study was to investigate the effect of receptor for advanced glycation end products (RAGE)-specific small interfering (si)RNA on the generation of proinflammatory cytokines in primary rat hepatic stellate cells (HSCs) and hepatic fibrotic (HF) rats. The RAGE-specific siRNA expression vector pAKD-GR126 was constructed, and then transfected into primary rat HSCs. Reverse transcription-quantitative polymerase chain reaction and western blot analyses were conducted to determine the mRNA and protein expression levels, respectively, of RAGE, tumor necrosis factor (TNF)-α and interleukin (IL)-6 in the primary HSCs. In addition, a CCl 4 -induced Sprague Dawley (SD) rat model of hepatic fibrosis was established, and pAKD-GR126 was injected into the SD rats via the tail vein. Serum TNF-α and IL-6 concentrations were determined using radioimmunoassay. The mRNA and protein expression levels of RAGE (mRNA, F=7.791; protein, F=36.513), TNF-α (mRNA, F=474.568; protein, F=123.500) and F=203.463; protein, F=320.555) in the pAKD-GR126-transfected primary HSCs were significantly reduced compared with those in the control and pAKD-NC groups (P<0.05). Serum TNF-α and IL-6 levels in the low-, medium-and high-dose pAKD-GR126 treatment groups were reduced compared with those in the fibrotic model group (TNF-α, F=416.397; IL-6, F=1,716.659; P<0.05). In summary, the RAGE-specific siRNA was able to effectively suppress the generation of the proinflammatory cytokines TNF-α and IL-6 in primary rat HSCs and HF rats.

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Role of the receptor for advanced glycation end products inhepatic fbrosis

Abstract: AIM:To study the role of advanced glycation end products (AGE) and their specific receptor (RAGE) in the pathogenesis of liver fibrogenesis.

Cited by 47 publications

References 51 publications

Can Pharmacological Targeting of Advanced Glycation End Products Provide Protection Against Experimentally Induced Liver Fibrosis?

Can Pharmacological Targeting of Advanced Glycation End Products Provide Protection Against Experimentally Induced Liver Fibrosis?

Involvement of the TAGE-RAGE system in non-alcoholic steatohepatitis: Novel treatment strategies

Small interfering RNA targeting receptor for advanced glycation end products suppresses the generation of proinflammatory cytokines

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