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Showing 1-30 of 37 results for "AB1252" within Papers
Hee-Yeon Kim et al.
British journal of pharmacology, 180(9), 1247-1266 (2022-12-09)
Paracetamol (acetaminophen)-induced hepatotoxicity is the leading cause of drug-induced liver injury worldwide. Autophagy is a degradative process by which various cargoes are collected by the autophagic receptors such as p62/SQSTM1/Sequestosome-1 for lysosomal degradation. Here, we investigated the protective role of
Ethanol and its Nonoxidative Metabolites Promote Acute Liver Injury by Inducing ER Stress, Adipocyte Death, and Lipolysis.
Park, et al.
Cellular and molecular gastroenterology and hepatology, 15, 281-306 (2023)
Mahir Bhardwaj et al.
ACS omega, 9(12), 13982-13993 (2024-04-01)
EIDD-1931 is the active form of molnupiravir, an orally effective drug approved by the United States Food and Drug Administration (USFDA) against COVID-19. Pharmacokinetic alteration can cause untoward drug interaction (drug-drug/disease-drug), but hardly any information is known about this recently
An-Ming Yang et al.
The Journal of clinical investigation, 127(7), 2829-2841 (2017-05-23)
Chronic liver disease with cirrhosis is the 12th leading cause of death in the United States, and alcoholic liver disease accounts for approximately half of all cirrhosis deaths. Chronic alcohol consumption is associated with intestinal bacterial dysbiosis, yet we understand
Hyon-Seung Yi et al.
PloS one, 10(5), e0127946-e0127946 (2015-05-30)
Accumulating evidence suggests that retinol and its metabolites are closely associated with liver fibrogenesis. Recently, we demonstrated that genetic ablation of alcohol dehydrogenase 3 (ADH3), a retinol metabolizing gene that is expressed in hepatic stellate cells (HSCs) and natural killer
Cristina Llorente et al.
Nature communications, 8(1), 837-837 (2017-10-19)
Chronic liver disease is rising in western countries and liver cirrhosis is the 12th leading cause of death worldwide. Simultaneously, use of gastric acid suppressive medications is increasing. Here, we show that proton pump inhibitors promote progression of alcoholic liver
Mark A Barnes et al.
Journal of leukocyte biology, 97(1), 161-169 (2014-11-16)
Recruitment of peripheral monocytes to the liver is a key contributor to the response to injury. MIF can act as a chemokine and cytokine, regulating innate immune responses in many tissues and cell types. We hypothesized that MIF contributes to
Simon Bucher et al.
Oxidative medicine and cellular longevity, 2018, 4396403-4396403 (2018-08-28)
Exposure to xenobiotics could favor the transition of nonalcoholic fatty liver (NAFL) to nonalcoholic steatohepatitis in obese patients. Recently, we showed in different models of NAFL that benzo[a]pyrene (B[a]P) and ethanol coexposure induced a steatohepatitis-like state. One model was HepaRG
Jacopo Baglieri et al.
The American journal of pathology, 191(9), 1564-1579 (2021-06-14)
Although hepatocellular cancer (HCC) usually occurs in the setting of liver fibrosis, the causal relationship between liver fibrosis and HCC is unclear. in vivo and in vitro models of HCC involving Colr/r mice (that produce a collagenase-resistant type I collagen) or wild-type
Koji Moriya et al.
Genes to cells : devoted to molecular & cellular mechanisms, 25(4), 257-269 (2020-02-06)
Most physiological changes follow a daily cycle in animals because their circadian rhythm is adjusted to and synchronized with sunlight. In particular, the circadian rhythm affects liver functions, including pharmacokinetics and metabolism. The influence of circadian rhythm has not been
Mohammed A Assiri et al.
Alcoholism, clinical and experimental research, 41(10), 1705-1714 (2017-08-15)
Chronic ethanol (EtOH) consumption is a major cause of liver disease worldwide. Oxidative stress is a known consequence of EtOH metabolism and is thought to contribute significantly to alcoholic liver disease (ALD). Therefore, elucidating pathways leading to sustained oxidative stress
Sachin Bhusari et al.
Toxicologic pathology, 43(8), 1114-1126 (2015-08-21)
The cell of origin of hepatoblastoma (HB) in humans and mice is unknown; it is hypothesized to be a transformed hepatocyte, oval cell, or hepatic progenitor cell. In mice, current dogma is that HBs arise from preexisting hepatocellular neoplasms as
Specification of fetal liver endothelial progenitors to functional zonated adult sinusoids requires c-Maf induction.
G??mez-Salinero, et al.
Cell Stem Cell, 29, 593-609 (2023)
Arnaud Tête et al.
Free radical biology & medicine, 129, 323-337 (2018-10-01)
We previously demonstrated that co-exposing pre-steatotic hepatocytes to benzo[a]pyrene (B[a]P), a carcinogenic environmental pollutant, and ethanol, favored cell death. Here, the intracellular mechanisms underlying this toxicity were studied. Steatotic WIF-B9 hepatocytes, obtained by a 48h-supplementation with fatty acids, were then
Zhihong Yang et al.
JCI insight, 6(16) (2021-08-24)
Alcohol-associated liver disease (ALD) represents a spectrum of histopathological changes, including alcoholic steatosis, steatohepatitis, and cirrhosis. One of the early responses to excessive alcohol consumption is lipid accumulation in the hepatocytes. Lipid ω-hydroxylation of medium- and long-chain fatty acid metabolized
Kyle J Thompson et al.
Alcohol and alcoholism (Oxford, Oxfordshire), 52(6), 629-637 (2017-10-17)
This study sought to compare mice bred to preferentially consume high amounts of alcohol (crossed-high alcohol preferring, cHAP) to c57BL/6 (C57) mice using a chronic-binge ethanol ingestion model to induce alcoholic liver disease (ALD). Male C57 and cHAP mice were
Pengcheng Wang et al.
Biochemical pharmacology, 145, 218-225 (2017-09-11)
Acetylation is the major metabolic pathway of isoniazid (INH) mediated by N-acetyltransferases (NATs). Previous reports suggest that slow acetylators have higher risks of INH hepatotoxicity than rapid acetylators, but the detailed mechanisms remain elusive. The current study used Nat1/2(-/-) mice
Camilla P Stice et al.
Archives of biochemistry and biophysics, 572, 81-88 (2015-01-17)
Chronic and excessive alcohol consumption leads to the development of alcoholic liver disease (ALD) and greatly increases the risk of liver cancer. Induction of the cytochrome p450 2E1 (CYP2E1) enzyme by chronic and excessive alcohol intake is known to play
Anuradha Ratna et al.
Hepatology communications, 5(7), 1165-1182 (2021-07-20)
Cellular stress-mediated chaperones are linked to liver macrophage activation and inflammation in alcohol-associated liver disease (ALD). In this study, we investigate the role of endoplasmic reticulum (ER) resident stress chaperone GP96/HSP90B1/GRP94, paralog of the HSP90 family, in ALD pathogenesis. We
S Vichi et al.
Toxicology in vitro : an international journal published in association with BIBRA, 30(1 Pt A), 176-184 (2015-03-22)
Within the Predict-IV FP7 project a strategy for measurement of in vitro biokinetics was developed, requiring the characterization of the cellular model used, especially regarding biotransformation, which frequently depends on cytochrome P450 (CYP) activity. The extrahepatic in situ CYP-mediated metabolism
Debanjan Dhar et al.
Cancer cell, 33(6), 1061-1077 (2018-06-13)
How fully differentiated cells that experience carcinogenic insults become proliferative cancer progenitors that acquire multiple initiating mutations is not clear. This question is of particular relevance to hepatocellular carcinoma (HCC), which arises from differentiated hepatocytes. Here we show that one
Chen Zhang et al.
Molecular medicine (Cambridge, Mass.), 27(1), 57-57 (2021-06-08)
Acetaminophen (APAP) overdose causes hepatotoxicity and even acute liver failure. Recent studies indicate that sterile inflammation and innate immune cells may play important roles in damage-induced hepatocytes regeneration and liver repair. The scavenger receptor CD36 has its crucial functions in
Won-Mook Choi et al.
Cell metabolism, 30(5), 877-889 (2019-09-03)
Activation of hepatocyte cannabinoid receptor-1 (CB1R) by hepatic stellate cell (HSC)-derived 2-arachidonoylglycerol (2-AG) drives de novo lipogenesis in alcoholic liver disease (ALD). How alcohol stimulates 2-AG production in HSCs is unknown. Here, we report that chronic alcohol consumption induced hepatic
Rebecca L McCullough et al.
Molecular immunology, 75, 122-132 (2016-06-10)
Complement is implicated in the development of alcoholic liver disease. C3 and C5 contribute to ethanol-induced liver injury; however, the role of C5a receptor (C5aR) on myeloid and non-myeloid cells to progression of injury is not known. C57BL/6 (WT), global
Xiaoxia Jin et al.
Frontiers in pharmacology, 9, 1317-1317 (2018-12-14)
This study was designed to explore the role of cytochrome P4502E1 (CYP2E1) expression in the course of brain edema induced by subacute poisoning with 1,2-dichloroethane (1,2-DCE). Mice were randomly divided into five groups: the control group, the 1,2-DCE poisoned group
Kuei-Chuan Lee et al.
American journal of physiology. Gastrointestinal and liver physiology, 316(5), G585-G597 (2019-03-01)
We investigated the migration of intestinal immune cells to the liver and their contribution to alcoholic liver disease. In mice fed ethanol, we found that an increased number of invariant natural killer T (iNKT) cells, which respond to the antigen
Moses New-Aaron et al.
Biology, 11(7) (2022-09-15)
Recently, we found that both HIV and acetaldehyde, an alcohol metabolite, induce hepatocyte apoptosis, resulting in the release of large extracellular vesicles called apoptotic bodies (ABs). The engulfment of these hepatocyte ABs by hepatic stellate cells (HSC) leads to their
Mohammad A Rahman et al.
Scientific reports, 9(1), 6571-6571 (2019-04-27)
Cellular CYP2E1 is well-known to mediate alcohol- (ALC) and acetaminophen- (APAP) induced toxicity in hepatic and extra-hepatic cells. Although exosomes have been gaining importance in understanding mechanism of intra- and inter-cellular communication, the functional role of drug metabolizing cytochrome P450
Demethylase JMJD6 as a New Regulator of Interferon Signaling: Effects of HCV and Ethanol Metabolism.
Murali Ganesan et al.
Cellular and molecular gastroenterology and hepatology, 5(2), 101-112 (2018-04-26)
Alcohol-induced progression of hepatitis C virus (HCV) infection is related to dysfunction of innate immunity in hepatocytes. Endogenously produced interferon (IFN)α induces activation of interferon-stimulated genes (ISGs) via triggering of the Janus kinase-signal transducer and activator of transcription 1 (STAT1)
Amruta Bhate et al.
Nature communications, 6, 8768-8768 (2015-11-05)
Although major genetic networks controlling early liver specification and morphogenesis are known, the mechanisms responsible for postnatal hepatic maturation are poorly understood. Here we employ global analyses of the mouse liver transcriptome to demonstrate that postnatal remodelling of the liver
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