SCC064

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Reduced cleavage of von willebrand factor by ADAMTS13 is associated with microangiopathic acute kidney injury following trauma.

William E Plautz et al.

Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis, 33(1), 14-24 (2021-12-11)

Acute kidney injury (AKI) is common after trauma, but contributory factors are incompletely understood. Increases in plasma von Willebrand Factor (vWF) with concurrent decreases in ADAMTS13 are associated with renal microvascular thrombosis in other disease states, but similar findings have

Alcohol Metabolism Potentiates HIV-Induced Hepatotoxicity: Contribution to End-Stage Liver Disease.

Murali Ganesan et al.

Biomolecules, 9(12) (2019-12-15)

In an era of improved survival due to modern antiretroviral therapy, liver disease has become a major cause of morbidity and mortality, resulting in death in 15-17% of human immunodeficiency virus (HIV)-infected patients. Alcohol enhances HIV-mediated liver damage and promotes

Honokiol Acts as a Potent Anti-Fibrotic Agent in the Liver through Inhibition of TGF-β1/SMAD Signaling and Autophagy in Hepatic Stellate Cells.

Seita Kataoka et al.

International journal of molecular sciences, 22(24) (2021-12-25)

Chronic liver injury may result in hepatic fibrosis, which can progress to cirrhosis and eventually liver failure. There are no drugs that are specifically approved for treating hepatic fibrosis. The natural product honokiol (HNK), a bioactive compound extracted from Magnolia

Interaction between estrogen receptor-α and PNPLA3 p.I148M variant drives fatty liver disease susceptibility in women.

Alessandro Cherubini et al.

Nature medicine, 29(10), 2643-2655 (2023-09-26)

Fatty liver disease (FLD) caused by metabolic dysfunction is the leading cause of liver disease and the prevalence is rising, especially in women. Although during reproductive age women are protected against FLD, for still unknown and understudied reasons some develop

Reparative and toxicity-reducing effects of liposome-encapsulated saikosaponin in mice with liver fibrosis.

Li-Yen Shiu et al.

Bioscience reports, 40(8) (2020-08-07)

Saikosaponin d (SSd), a primary active component of the Chinese herb Bupleurum falcatum, has antitumor and antiliver fibrosis effects. However, the toxicity of SSd at high doses can induce conditions such as metabolic disorders and hemolysis in vivo, thus hampering

Bouchardatine analogue alleviates non-alcoholic hepatic fatty liver disease/non-alcoholic steatohepatitis in high-fat fed mice by inhibiting ATP synthase activity.

Yong Rao et al.

British journal of pharmacology, 176(16), 2877-2893 (2019-05-22)

Non-alcoholic hepatic fatty liver disease (NAFLD) is a manifestation of the metabolic syndrome in the liver and non-alcoholic steatohepatitis (NASH) represents its advanced stage. R17 derived from bouchardatine, shows benefits in the metabolic syndrome, but has not been tested in

Human hepatic stellate cell lines, LX-1 and LX-2: new tools for analysis of hepatic fibrosis.

Xu, L, et al.

Gut, 54, 142-151 (2005)

Collagen release by human hepatic stellate cells requires vitamin C and is efficiently blocked by hydroxylase inhibition.

Natalia Smith-Cortinez et al.

FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 35(2), e21219-e21219 (2020-11-26)

Liver fibrosis is characterized by the accumulation of extracellular matrix proteins, mainly composed of collagen. Hepatic stellate cells (HSCs) mediate liver fibrosis by secreting collagen. Vitamin C (ascorbic acid) is a cofactor of prolyl-hydroxylases that modify newly synthesized collagen on

SAA1/TLR2 axis directs chemotactic migration of hepatic stellate cells responding to injury.

Anteneh Getachew et al.

iScience, 24(5), 102483-102483 (2021-06-12)

Hepatic stellate cells (HSCs) are crucial for liver injury repair and cirrhosis. However, the mechanism of chemotactic recruitment of HSCs into injury loci is still largely unknown. Here, we demonstrate that serum amyloid A1 (SAA1) acts as a chemokine recruiting

Exosomal Transmission of MicroRNA from HCV Replicating Cells Stimulates Transdifferentiation in Hepatic Stellate Cells.

Ji Hyun Kim et al.

Molecular therapy. Nucleic acids, 14, 483-497 (2019-02-13)

The mechanism by which hepatitis C virus (HCV) causes fibrosis and other chronic liver diseases remains poorly understood. Previously, we observed that HCV infection induces microRNA-192 (miR-192) expression, which in turn upregulates transforming growth factor β1 (TGF-β1) in hepatocytes. In

mir-101-3p Downregulation Promotes Fibrogenesis by Facilitating Hepatic Stellate Cell Transdifferentiation During Insulin Resistance.

Marica Meroni et al.

Nutrients, 11(11) (2019-11-02)

Insulin resistance (IR) and microRNAs (miRNAs), which regulate cell-to-cell communication between hepatocytes and hepatic stellate cells (HSCs), may intertwine in nonalcoholic fatty liver disease (NAFLD) pathogenesis. The aim of this study was to evaluate whether epigenetics and environmental factors interact

White Button Mushroom Extracts Modulate Hepatic Fibrosis Progression, Inflammation, and Oxidative Stress In Vitro and in LDLR-/- Mice.

Paloma Gallego et al.

Foods (Basel, Switzerland), 10(8) (2021-08-28)

Liver fibrosis can be caused by non-alcoholic steatohepatitis (NASH), among other conditions. We performed a study to analyze the effects of a nontoxic, water-soluble extract of the edible mushroom Agaricus bisporus (AB) as a potential inhibitor of fibrosis progression in

Simultaneous Induction of Glycolysis and Oxidative Phosphorylation during Activation of Hepatic Stellate Cells Reveals Novel Mitochondrial Targets to Treat Liver Fibrosis.

Natalia Smith-Cortinez et al.

Cells, 9(11) (2020-11-15)

Upon liver injury, hepatic stellate cells (HSCs) transdifferentiate to migratory, proliferative and extracellular matrix-producing myofibroblasts (e.g., activated HSCs; aHSCs) causing liver fibrosis. HSC activation is associated with increased glycolysis and glutaminolysis. Here, we compared the contribution of glycolysis, glutaminolysis and

Targeting oxidized phospholipids by AAV-based gene therapy in mice with established hepatic steatosis prevents progression to fibrosis.

Clint M Upchurch et al.

Science advances, 8(28), eabn0050-eabn0050 (2022-07-21)

Oxidized phosphatidylcholines (OxPCs) are implicated in chronic tissue damage. Hyperlipidemic LDL-R--deficient mice transgenic for an OxPC-recognizing IgM fragment (scFv-E06) are protected against nonalcoholic fatty liver disease (NAFLD). To examine the effect of OxPC elimination at different stages of NAFLD progression

Expression of Septin4 in human hepatic stellate cells LX-2 stimulated by LPS.

Sun, Xiaolei, et al.

Inflammation, 36, 539-548 (2013)

Inhibiting IRE1α-endonuclease activity decreases tumor burden in a mouse model for hepatocellular carcinoma.

Nataša Pavlović et al.

eLife, 9 (2020-10-27)

Hepatocellular carcinoma (HCC) is a liver tumor that usually arises in patients with cirrhosis. Hepatic stellate cells are key players in the progression of HCC, as they create a fibrotic micro-environment and produce growth factors and cytokines that enhance tumor

A blocking monoclonal antibody to CCL24 alleviates liver fibrosis and inflammation in experimental models of liver damage.

Michal Segal-Salto et al.

JHEP reports : innovation in hepatology, 2(1), 100064-100064 (2020-02-11)

C-C motif chemokine ligand 24 (CCL24) is a chemokine that regulates inflammatory and fibrotic activities through its receptor, C-C motif chemokine receptor (CCR3). The aim of the study was to evaluate the involvement of the CCL24-CCR3 axis in liver fibrosis

Myofibroblast-specific YY1 promotes liver fibrosis.

Huan Liu et al.

Biochemical and biophysical research communications, 514(3), 913-918 (2019-05-16)

Liver fibrosis is a common consequence of various chronic hepatitis and liver injuries. The myofibroblasts, through the accumulation of extracellular matrix (ECM) proteins, are closely associated with the progression of liver fibrosis. However, the molecular mechanisms underlying transcriptional regulation of

Extracellular PKM2 facilitates organ-tissue fibrosis progression.

Hongwei Han et al.

iScience, 24(10), 103165-103165 (2021-10-26)

Persistent activation of fibroblasts and resistance of myofibroblasts to turnover play important roles in organ-tissue fibrosis development and progression. The mechanism that mediates apoptosis resistance of myofibroblasts is not understood. Here, we report that myofibroblasts express and secrete PKM2. Extracellular PKM2

Discovery of 3,7-dimethoxyflavone that inhibits liver fibrosis based on dual mechanisms of antioxidant and inhibitor of activated hepatic stellate cell.

Hyomin Park et al.

Free radical biology & medicine, 204, 195-206 (2023-05-06)

The important pathway toward liver fibrosis is the TGF-β1-induced activation of hepatic stellate cells (HSCs). To discover chemicals to inhibit liver fibrosis, we screened 3000 chemicals using cell array system where human HSCs line LX2 cells are activated with TGF-β1.

Myostatin as a fibroblast-activating factor impacts on postoperative outcome in patients with hepatocellular carcinoma.

Sachiyo Yoshio et al.

Hepatology research : the official journal of the Japan Society of Hepatology, 51(7), 803-812 (2021-05-18)

In patients with liver cirrhosis, high levels of serum myostatin are associated with poor prognosis. We aimed to clarify the influence of myostatin on the prognosis of patients with non-alcoholic fatty liver disease-hepatocellular carcinoma (NAFLD-HCC) without cirrhosis and on the

HK1 from hepatic stellate cell-derived extracellular vesicles promotes progression of hepatocellular carcinoma.

Qi-Tao Chen et al.

Nature metabolism, 4(10), 1306-1321 (2022-10-04)

Extracellular vesicles play crucial roles in intercellular communication in the tumor microenvironment. Here we demonstrate that in hepatic fibrosis, TGF-β stimulates the palmitoylation of hexokinase 1 (HK1) in hepatic stellate cells (HSCs), which facilitates the secretion of HK1 via large extracellular

Sulforaphane Inhibits the Expression of Long Noncoding RNA H19 and Its Target APOBEC3G and Thereby Pancreatic Cancer Progression.

Yiqiao Luo et al.

Cancers, 13(4) (2021-03-07)

Pancreatic ductal adenocarcinoma (PDAC) is extremely malignant and the therapeutic options available usually have little impact on survival. Great hope is placed on new therapeutic targets, including long noncoding RNAs (lncRNAs), and on the development of new drugs, based on

5-methoxytryptophan alleviates liver fibrosis by modulating FOXO3a/miR-21/ATG5 signaling pathway mediated autophagy.

Ming Tong et al.

Cell cycle (Georgetown, Tex.), 20(7), 676-688 (2021-03-19)

Liver fibrosis is a critical health issue in the world due to its rapidly increasing prevalence. It is of great demand to develop effective drugs for the treatment of liver fibrosis. 5-methoxytryptophan (5-MTP) has been reported to play an important

The Fibronectin-ILT3 Interaction Functions as a Stromal Checkpoint that Suppresses Myeloid Cells.

Kevin J Paavola et al.

Cancer immunology research, 9(11), 1283-1297 (2021-08-25)

Suppressive myeloid cells inhibit antitumor immunity by preventing T-cell responses. Immunoglobulin-like transcript 3 (ILT3; also known as LILRB4) is highly expressed on tumor-associated myeloid cells and promotes their suppressive phenotype. However, the ligand that engages ILT3 within the tumor microenvironment

Peritumoral activated hepatic stellate cells are associated with hepatic recurrence for resectable colorectal adenocarcinoma liver metastasis following resection.

Li Deng et al.

Oncology letters, 20(6), 287-287 (2020-10-06)

The formation of the pre-metastatic niche (PMN), which precedes the establishment of tumor lesions, plays a critical role in cancer recurrence and metastasis. Hepatic stellate cells (HSCs), a critical liver stromal cell component, can be induced to facilitate metastasis by

Green synthesis of fluorescent carbon nanodots from sage leaves for selective anticancer activity on 2D liver cancer cells and 3D multicellular tumor spheroids.

Shadi Sawalha et al.

Nanoscale advances, 5(21), 5974-5982 (2023-10-26)

Carbon nanodots, a family of carbon-based nanomaterials, have been synthesized through different methods from various resources, affecting the properties of the resulting product and their application. Herein, carbon nanodots (CNDs) were synthesized with a green and simple hydrothermal method from

Epigenetic regulation of connective tissue growth factor by microRNA-214 delivery in exosomes from mouse or human hepatic stellate cells.

Chen, Li, et al.

Hepatology (2013)

A Positive Feedback Loop of TET3 and TGF-β1 Promotes Liver Fibrosis.

Yetao Xu et al.

Cell reports, 30(5), 1310-1318 (2020-02-06)

Pathological activation of TGF-β signaling is universal in fibrosis. Aberrant TGF-β signaling in conjunction with transdifferentiation of hepatic stellate cells (HSCs) into fibrogenic myofibroblasts plays a central role in liver fibrosis. Here we report that the DNA demethylase TET3 is

Modeling Progressive Fibrosis with Pluripotent Stem Cells Identifies an Anti-fibrotic Small Molecule.

Preethi Vijayaraj et al.

Cell reports, 29(11), 3488-3505 (2019-12-12)

Progressive organ fibrosis accounts for one-third of all deaths worldwide, yet preclinical models that mimic the complex, progressive nature of the disease are lacking, and hence, there are no curative therapies. Progressive fibrosis across organs shares common cellular and molecular

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