Influence of HLA‐B18 on liver fibrosis progression in a cohort of HIV/HCV coinfected individuals

Bavaro, Davide Fiore; Saracino, Annalisa; Fiordelisi, Deborah; Bruno, Giuseppe; Ladisa, Nicoletta; Monno, Laura; Angarano, Gioacchino

doi:10.1002/jmv.25385

Cited by 2 publications

(1 citation statement)

References 35 publications

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“…Notably, HIV has a direct role in liver damage, increasing the risk of cirrhosis in patients with chronic hepatitis viruses infection, alcoholic hepatitis, and non-alcoholic fat liver disease (NAFLD) [125][126][127]. Indeed, HIV viral envelope can interact with hepatocytes enhancing ROS production and oxidative stress; this, in turn, promotes a pro-fibrogenic environment, with activation of the TGFβ1 pathway and secretion of extracellular matrix by stellate cells [128,129].…”

Section: Liver Diseasementioning

confidence: 99%

A Step Closer to the “Fourth 90”: A Practical Narrative Review of Diagnosis and Management of Nutritional Issues of People Living with HIV

et al. 2021

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The quality of life of people living with HIV (PLWH) has remarkably increased thanks to the introduction of combined antiretroviral therapy. Still, PLWH are exposed to an increased risk of cardiovascular diseases, diabetes, chronic kidney disease, and liver disease. Hence, the purpose of this review is to summarize the current knowledge about diagnosis and nutritional management with specific indication of macro and micronutrients intake for the main comorbidities of PLWH. In fact, a prompt diagnosis and management of lifestyle behaviors are fundamental steps to reach the “fourth 90”. To achieve an early diagnosis of these comorbidities, clinicians have at their disposal algorithms such as the Framingham Score to assess cardiovascular risk; transient elastography and liver biopsy to detect NAFLD and NASH; and markers such as the oral glucose tolerance test and GFR to identify glucose impairment and renal failure, respectively. Furthermore, maintenance of ideal body weight is the goal for reducing cardiovascular risk and to improve diabetes, steatosis and fibrosis; while Mediterranean and low-carbohydrate diets are the dietetic approaches proposed for cardioprotective effects and for glycemic control, respectively. Conversely, diet management of chronic kidney disease requires different nutritional assessment, especially regarding protein intake, according to disease stage and eventually concomitant diabetes.

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Section: Liver Diseasementioning

confidence: 99%

A Step Closer to the “Fourth 90”: A Practical Narrative Review of Diagnosis and Management of Nutritional Issues of People Living with HIV

et al. 2021

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Effect of NLRC5 on activation and reversion of hepatic stellate cells by regulating the nuclear factor-κB signaling pathway

Zhang¹,

Yao²,

Zhang³

et al. 2019

WJG

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BACKGROUND The formation of liver fibrosis is mainly caused by the activation of hepatic stellate cells (HSCs) and the imbalance of extracellular matrix (ECM) production and degradation. The treatment of liver fibrosis mainly includes removing the cause, inhibiting the activation of HSCs, and inhibiting inflammation. NOD-like receptor (NLR) family, caspase activation and recruitment domain (CARD) domain containing 5/NOD27/CLR16.1 (NLRC5) is a highly conserved member of the NLR family and is involved in inflammation and immune responses by regulating various signaling pathways such as nuclear factor-κB (NF-κB) signaling. It has been found that NLRC5 plays an important role in liver fibrosis, but its specific effect and possible mechanism remain to be fully elucidated. AIM To investigate the role of NLRC5 in the activation and reversion of HSCs induced with transforming growth factor-β (TGF-β) and MDI, and to explore its relationship with liver fibrosis. METHODS A total of 24 male C57BL/6 mice were randomly divided into three groups, including normal, fibrosis, and recovery groups. Twenty-four hours after a liver fibrosis and spontaneous reversion model was established, the mice were sacrificed and pathological examination of liver tissue was performed to observe the degree of liver fibrosis in each group. LX-2 cells were cultured in vitro and treated with TGF-β1 and MDI. Real-time quantitative PCR (qPCR) and Western blot were used to analyze the expression levels of NLRC5, α-smooth muscle actin (α-SMA), and collagen type I alpha1 (Col1a1) in each group. The activity of NF-κB in each group of cells transfected with NLRC5-siRNA was detected. RESULTS Compared with the normal mice, the expression level of NLRC5 increased significantly ( P < 0.01) in the fibrosis group, but decreased significantly in the recovery group ( P < 0.01). In in vitro experiments, the content of NLRC5 was enhanced after TGF-β1 stimulation and decreased to a lower level when treated with MDI ( P < 0.01). The expression of α-SMA and Col1a1 proteins and mRNAs in TGF-β1-mediated cells was suppressed by transfection with NLRC5-siRNA ( P < 0.01). Western blot analysis showed that the expression of NF-κB p65 protein and phosphorylated IκBα (p-IκBα) was increased in the liver of mice in the fibrosis group but decreased in the recovery group ( P < 0.01), and the protein level of nuclear p65 and p-IκBα was significantly increased after treatment with NLRC5-siRNA ( P < 0.01). CONCLUSION NLRC5 may play a key role in the development and reversal of hepatic fibrosis through the NF-κB signaling pathway, and it is expected to be one of the clinical therapeutic targets.

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Influence of HLA‐B18 on liver fibrosis progression in a cohort of HIV/HCV coinfected individuals

Cited by 2 publications

References 35 publications

A Step Closer to the “Fourth 90”: A Practical Narrative Review of Diagnosis and Management of Nutritional Issues of People Living with HIV

A Step Closer to the “Fourth 90”: A Practical Narrative Review of Diagnosis and Management of Nutritional Issues of People Living with HIV

Effect of NLRC5 on activation and reversion of hepatic stellate cells by regulating the nuclear factor-κB signaling pathway

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