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10. Branched-Chain Amino Acids in Liver Diseases: Complexity and Controversy.

Author

Zhang, Yaqi, Zhan, Luqi, Zhang, Lingjian, Shi, Qingmiao, and Li, Lanjuan

Abstract

Branched-chain amino acids (BCAAs), as essential amino acids, engage in various physiological processes, such as protein synthesis, energy supply, and cellular signaling. The liver is a crucial site for BCAA metabolism, linking the changes in BCAA homeostasis with the pathogenesis of a variety of liver diseases and their complications. Peripheral circulating BCAA levels show complex trends in different liver diseases. This review delineates the alterations of BCAAs in conditions including non-alcoholic fatty liver disease, hepatocellular carcinoma, cirrhosis, hepatic encephalopathy, hepatitis C virus infection, and acute liver failure, as well as the potential mechanisms underlying these changes. A significant amount of clinical research has utilized BCAA supplements in the treatment of patients with cirrhosis and liver cancer. However, the efficacy of BCAA supplementation in clinical practice remains uncertain and controversial due to the heterogeneity of studies. This review delves into the complicated relationship between BCAAs and liver diseases and tries to untangle what role BCAAs play in the occurrence, development, and outcomes of liver diseases. [ABSTRACT FROM AUTHOR]

Published
2024
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16. Additional file 2 of SGOL2 is a novel prognostic marker and fosters disease progression via a MAD2-mediated pathway in hepatocellular carcinoma

Author

Hu, Qingqing, Liu, Qiuhong, Zhao, Yalei, Zhang, Lingjian, and Li, Lanjuan

Abstract

Additional file 2: Fig. S1. High expression of SGOL2 in HCC in public database. Fig. S2. The mRNA and protein levels of SGOL1 after the knockdown of SGOL2 in HCC cell lines. Fig. S3. Subgroup expression analysis of SGOL2 in HCC. Fig. S4. Elevated expression of SGOL2 indicated a poor prognosis in HCC patients. Fig. S5. SGOL2 mutations and the associations between SGOL2 and immune cells in HCC. Fig. S6. Genes related to SGOL2 or MAD2 in HCC. Fig. S7. Hub gene analysis. Fig. S8. The predicted transcription factors binding to SGOL2 or MAD2.

Published
2022
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26. Aneurysm and Artery Dissection Following the use of Vascular Endothelial Growth Factor Inhibitor: A Real-World Analysis Using a Spontaneous Reporting System

Author

Jian Gong, WANG Shuyue, CHEN Mingzhu, ZHANG Xinghui, ZHANG Lingjian, JIA Min, SHEN Zhiwen, WANG Junyan, XU Jing, ZHENG Zheng, WANG Mengmeng, LV Xuanrui, ZONG Xiaoyu, LI Hui, ZHOU Jin, MENG Tong, Bin Zhao, and GONG Jian

Abstract

Background: There are few real-world studies comparing the incidence, clinical features, and prognosis of aneurysm and artery dissection related to various vascular endothelial growth factor inhibitor (VPI) regimens. This study evaluated the recent evidence of aneurysm and artery dissection after VPI therapy. The purpose was to evaluate and compare the links between different VPIs and aneurysm and artery dissection by investigating the Food and Drug Administration Adverse Event Reporting System (FAERS).Methods: Using FAERS data from January 2004 to March 2020, disproportionality analysis was used for data mining to screen suspected aneurysm and artery dissection cases after different VPI treatments. The times to onset and fatality rates of suspected drugs were also investigated to assess prognoses.Results: In total, there were 634 reports of aneurysm and artery dissection events after VPI. Ramucirumab appeared to have a stronger association than other VPIs, based on the reporting odds ratio (ROR = 3.68, 95% [2.18, 6.23]). The results showed a significant difference in onset time (P < 0.001), and a quick onset occurred in 60.13% of cases. The median time to aneurysm and artery dissection was 79.5 (IQR: 19–273.5) days after VPI administration. The results also showed that men were more affected than women (59.68% vs. 40.32%), and patients older than 45 years were more affected than younger patients (68.12% vs. 3.93%). Finally, the suspected drugs generally led to a 19.98% fatality rate and a 29.81% hospitalization rate. The highest death rate was associated with Aflibercept (25.49%).Conclusions: We identified signals for aneurysm and artery dissection following various VPIs in real-world practice using the FAERS, which represents the first step for continued pharmacovigilance investigation.

Published
2020

31. Two new antitumor constituents from a soil fungus Curvularia inaequalis (strain HS-FG-257)

Author

Ji-Dong Wang, Fang Jiashuang, Qian-Feng Liu, Wensheng Xiang, Hui Zhang, Zhang Lingjian, Yan-Wei Pang, and Xiangjing Wang

Subjects
Pharmacology, Antifungal, China, Molecular Structure, Curvularia inaequalis, medicine.drug_class, Antiparasitic, Antineoplastic Agents, Biology, Microbiology, Beta-lactam, chemistry.chemical_compound, Ascomycota, Soil fungus, chemistry, Cell Line, Tumor, Drug Discovery, Botany, medicine, Humans, Biological Assay, Soil Microbiology
Abstract

Two new antitumor constituents from a soil fungus Curvularia inaequalis (strain HS-FG-257)

Published
2013

32. Knockdown of CXCL1 improves ACLF by reducing neutrophil recruitment to attenuate ROS production and hepatocyte apoptosis.

Author

Tang S, Zhang J, Zhang L, Zhao Y, Xiao L, Zhang F, Li Q, Yang Y, Liu Q, Xu J, and Li L

Subjects
Animals, Mice, Apoptosis genetics, Cytokines, Hepatocytes, Neutrophil Infiltration, Reactive Oxygen Species, Acute-On-Chronic Liver Failure genetics
Abstract

Background: Acute-on-chronic liver failure (ACLF) is an acute decompensated syndrome based on chronic liver disease, while neutrophil recruitment is the most critical early step. C-X-C motif chemokine ligand 1 (CXCL1), a cytokine that recruits neutrophils, was significantly upregulated in both ACLF mice and patients with ACLF. This present study aims to explore the role of CXCL1 in the pathogenesis of ACLF., Methods: We established an ACLF mouse model induced by carbon tetrachloride, lipopolysaccharide, and D-galactosamine, and used adeno-associated virus to achieve overexpression and knockdown of Cxcl1. We employed mass cytometry, flow cytometry, multiplex cytokine and chemokine analysis, Western blot, and reactive oxygen species (ROS) detection in mice blood and liver. ACLF patients (n = 10) and healthy controls (n = 5) were included, and their liver samples were stained using multiplex immunohistochemistry techniques., Results: CXCL1 was significantly elevated in both ACLF mice and patients. CXCL1 recruits neutrophils by binding to the C-X-C motif chemokine receptor 2 on the surface of neutrophils, affects ACLF prognosis by generating ROS and mitochondrial depolarization and modulating caspase3-related apoptotic pathways. We found that the knockdown of CXCL1 attenuated the infiltration of neutrophils in the mouse liver, reduced the expression of inflammatory cytokines, and also significantly downregulated ROS production and caspase3-related hepatocyte apoptosis, thereby ameliorating the liver injury of ACLF., Conclusions: CXCL1 is a core player in the mobilization of neutrophils in ACLF, and the knockdown of Cxcl1 improves neutrophil infiltration, reduces ROS levels, and reduces hepatocyte apoptosis, thereby attenuating inflammation and liver injury in ACLF. Our results revealed a previously unknown link between CXCL1-induced neutrophil recruitment and ACLF, providing evidencing for potential therapies targeting ACLF., (Copyright © 2023 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the American Association for the Study of Liver Diseases.)

Published
2023
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