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The mechanism of HBx protein to promote the initiation and progression of hepatocellular carcinoma

initiating the proliferation of HBV [ 15 ]. Duan et al. found that HBx protein can increase intracellular oxidative stress and activate the transcription factors signal transducer and activator of transcription (STAT3), nuclear factor kappa B (NFκB), and other factors by causing mitochondrial damage, which results in the acceleration of hepatoma cell proliferation [ 15 ]. Long noncoding RNA high expression in HCC (lncRNA-HEIH) is a carcinogenic lncRNA overexpressed in hepatoma. It accelerates the malignant progression of hepatoma by promoting the abnormal proliferation

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Role of SR-BI in atherosclerosis, malignancies, and infectious diseases

plaques and interacts with ATP-binding cassette transporter A1 (ABCA1), ATP-binding cassette transporter G1 (ABCG1), and SR-BI, causing macrophages with excessive lipids to clear cholesterol through RCT and transport it to the liver [ 9 ]. The complex network of programs that triggers cholesterol homeostasis occurs predominantly in the liver. Therefore, the liver is considered a “power station” of metabolism. Dietary cholesterol is transported from the intestine to the liver through HDLs, and all HDL particles are internalized in the liver after interacting with

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Autophagy and virus infection

limit DNA damage and chromosome instability. However, the specific mechanism remains unclear [ 14 ]. Autophagy can be also regarded as a non-apoptotic programmed cell death process [ 15 ]. 3 Autophagy and virus infection Autophagy can eliminate invading pathogens in a process called as autophagocytosis. For several virus infections, autophagy can keep its titer in the body at low levels [ 16 ]. Several studies have shown that autophagy can weaken encephalitis induced by Sindbis virus [ 17 ]. The capsid protein of Sindbis virus is recruited on autophagosome

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Research progress of cholangiocarcinoma induced by liver fluke infection

recurrent ulcer of the bile duct wall. Pinlaor et al . [ 27 ] presented that the expression levels of the mRNA of inducible nitrogen oxide synthase, antioxidase mRNA, and nuclear factor-κB detected from the host infected by O . viverrini were significantly increased. Similarly, the levels of nitric oxide end product, malondialdehyde, and plasma nitrate were increased significantly. This result indicates that liver fluke infection stimulates host cells to produce oxidative and nitridation reactions, resulting in the injury and repair of epithelial cells of the bile

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