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Article: Augmented Liver Uptake of the Membrane Voltage Sensor Tetraphenylphosphonium Distinguishes Early Fibrosis in a Mouse Model.

Pandita, Himanshi / Mezey, Esteban / Ganapathy-Kanniappan, Shanmugasundaram

2021 Volume 12, Page(s) 676722

Abstract: Mitochondrial (mito-) oxidative phosphorylation (OxPhos) is a critical determinant of cellular membrane potential/voltage. Dysregulation of OxPhos is a biochemical signature of advanced liver fibrosis. However, less is known about the net voltage of the ... ...

Abstract	Mitochondrial (mito-) oxidative phosphorylation (OxPhos) is a critical determinant of cellular membrane potential/voltage. Dysregulation of OxPhos is a biochemical signature of advanced liver fibrosis. However, less is known about the net voltage of the liver in fibrosis. In this study, using the radiolabeled [
Language	English
Publishing date	2021-10-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2021.676722
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Article ; Online: Abnormal liver chemistries as a predictor of COVID-19 severity and clinical outcomes in hospitalized patients.

Krishnan, Arunkumar / Prichett, Laura / Tao, Xueting / Alqahtani, Saleh A / Hamilton, James P / Mezey, Esteban / Strauss, Alexandra T / Kim, Ahyoung / Potter, James J / Chen, Po-Hung / Woreta, Tinsay A

World journal of gastroenterology

2022 Volume 28, Issue 5, Page(s) 570–587

Abstract: Background: Abnormal liver chemistries are common findings in patients with Coronavirus Disease 2019 (COVID-19). However, the association of these abnormalities with the severity of COVID-19 and clinical outcomes is poorly understood.: Aim: We aimed ... ...

Abstract	Background: Abnormal liver chemistries are common findings in patients with Coronavirus Disease 2019 (COVID-19). However, the association of these abnormalities with the severity of COVID-19 and clinical outcomes is poorly understood. Aim: We aimed to assess the prevalence of elevated liver chemistries in hospitalized patients with COVID-19 and compare the serum liver chemistries to predict the severity and in-hospital mortality. Methods: This retrospective, observational study included 3380 patients with COVID-19 who were hospitalized in the Johns Hopkins Health System (Baltimore, MD, United States). Demographic data, clinical characteristics, laboratory findings, treatment measures, and outcome data were collected. Cox regression modeling was used to explore variables associated with abnormal liver chemistries on admission with disease severity and prognosis. Results: A total of 2698 (70.4%) had abnormal alanine aminotransferase (ALT) at the time of admission. Other more prevalent abnormal liver chemistries were aspartate aminotransferase (AST) (44.4%), alkaline phosphatase (ALP) (16.1%), and total bilirubin (T-Bil) (5.9%). Factors associated with liver injury were older age, Asian ethnicity, other race, being overweight, and obesity. Higher ALT, AST, T-Bil, and ALP levels were more commonly associated with disease severity. Multivariable adjusted Cox regression analysis revealed that abnormal AST and T-Bil were associated with the highest mortality risk than other liver injury indicators during hospitalization. Abnormal AST, T-Bil, and ALP were associated with a need for vasopressor drugs, whereas higher levels of AST, T-Bil, and a decreased albumin levels were associated with mechanical ventilation. Conclusion: Abnormal liver chemistries are common at the time of hospital admission in COVID-19 patients and can be closely related to the patient's severity and prognosis. Elevated liver chemistries, specifically ALT, AST, ALP, and T-Bil levels, can be used to stratify risk and predict the need for advanced therapies in these patients.
MeSH term(s)	Alanine Transaminase ; Alkaline Phosphatase ; Aspartate Aminotransferases ; Baltimore ; Bilirubin ; COVID-19/diagnosis ; COVID-19/therapy ; Hospitalization ; Humans ; Liver/chemistry ; Retrospective Studies ; Severity of Illness Index
Chemical Substances	Aspartate Aminotransferases (EC 2.6.1.1) ; Alanine Transaminase (EC 2.6.1.2) ; Alkaline Phosphatase (EC 3.1.3.1) ; Bilirubin (RFM9X3LJ49)
Language	English
Publishing date	2022-03-22
Publishing country	United States
Document type	Journal Article ; Observational Study
ZDB-ID	2185929-2
ISSN	2219-2840 ; 1007-9327
ISSN (online)	2219-2840
ISSN	1007-9327
DOI	10.3748/wjg.v28.i5.570
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Article ; Online: Global burden of disease: acute-on-chronic liver failure, a systematic review and meta-analysis.

Mezzano, Gabriel / Juanola, Adria / Cardenas, Andres / Mezey, Esteban / Hamilton, James P / Pose, Elisa / Graupera, Isabel / Ginès, Pere / Solà, Elsa / Hernaez, Ruben

Gut

2021 Volume 71, Issue 1, Page(s) 148–155

Abstract: Background and aims: Acute-on-chronic liver failure (ACLF) is characterised by acute decompensation of cirrhosis associated with organ failures. We systematically evaluated the geographical variations of ACLF across the world in terms of prevalence, ... ...

Abstract	Background and aims: Acute-on-chronic liver failure (ACLF) is characterised by acute decompensation of cirrhosis associated with organ failures. We systematically evaluated the geographical variations of ACLF across the world in terms of prevalence, mortality, aetiology of chronic liver disease (CLD), triggers and organ failures. Methods: We searched EMBASE and PubMed from 3/1/2013 to 7/3/2020 using the ACLF-EASL-CLIF (European Association for the Study of the Liver-Chronic Liver Failure) criteria. Two investigators independently conducted the abstract selection/abstraction of the aetiology of CLD, triggers, organ failures and prevalence/mortality by presence/grade of ACLF. We grouped countries into Europe, East/South Asia and North/South America. We calculated the pooled proportions, evaluated the methodological quality using the Newcastle-Ottawa Scale and statistical heterogeneity, and performed sensitivity analyses. Results: We identified 2369 studies; 30 cohort studies met our inclusion criteria (43 206 patients with ACLF and 140 835 without ACLF). The global prevalence of ACLF among patients admitted with decompensated cirrhosis was 35% (95% CI 33% to 38%), highest in South Asia at 65%. The global 90-day mortality was 58% (95% CI 51% to 64%), highest in South America at 73%. Alcohol was the most frequently reported aetiology of underlying CLD (45%, 95% CI 41 to 50). Infection was the most frequent trigger (35%) and kidney dysfunction the most common organ failure (49%). Sensitivity analyses showed regional estimates grossly unchanged for high-quality studies. Type of design, country health index, underlying CLD and triggers explained the variation in estimates. Conclusions: The global prevalence and mortality of ACLF are high. Region-specific variations could be explained by the type of triggers/aetiology of CLD or grade. Health systems will need to tailor early recognition and treatment of ACLF based on region-specific data.
MeSH term(s)	Acute-On-Chronic Liver Failure/epidemiology ; Global Burden of Disease ; Humans ; Infections/epidemiology ; Liver Diseases, Alcoholic/epidemiology ; Prevalence ; Renal Insufficiency/epidemiology
Language	English
Publishing date	2021-01-12
Publishing country	England
Document type	Journal Article ; Meta-Analysis ; Research Support, Non-U.S. Gov't ; Systematic Review
ZDB-ID	80128-8
ISSN	1468-3288 ; 0017-5749
ISSN (online)	1468-3288
ISSN	0017-5749
DOI	10.1136/gutjnl-2020-322161
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Article ; Online: Increased ethanol-inducible cytochrome P450-2E1 and cytochrome P450 isoforms in exosomes of alcohol-exposed rodents and patients with alcoholism through oxidative and endoplasmic reticulum stress.

Cho, Young-Eun / Mezey, Esteban / Hardwick, James P / Salem, Norman / Clemens, Dahn L / Song, Byoung-Joon

Hepatology communications

2017 Volume 1, Issue 7, Page(s) 675–690

Abstract: This study investigated the role of ethanol-inducible cytochrome P450-2E1 (CYP2E1) in enhancing CYP2E1 and other P450 proteins in extracellular vesicles (EVs) from alcohol-exposed rodents and human patients with alcoholism and their effects on oxidative ... ...

Abstract	This study investigated the role of ethanol-inducible cytochrome P450-2E1 (CYP2E1) in enhancing CYP2E1 and other P450 proteins in extracellular vesicles (EVs) from alcohol-exposed rodents and human patients with alcoholism and their effects on oxidative hepatocyte injury. Female Fischer rats and wild-type or
Language	English
Publishing date	2017-07-13
Publishing country	United States
Document type	Journal Article
ISSN	2471-254X
ISSN (online)	2471-254X
DOI	10.1002/hep4.1066
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Article ; Online: Is the pathway of energy metabolism modified in advanced cirrhosis?

Ganapathy-Kanniappan, Shanmugasundaram / Karthikeyan, Swathi / Geschwind, Jean-Francois / Mezey, Esteban

Journal of hepatology

2014 Volume 61, Issue 2, Page(s) 452

MeSH term(s)	Adenosine Triphosphate/metabolism ; Animals ; Chemical and Drug Induced Liver Injury/metabolism ; Glycolysis/physiology ; Hepatocytes/metabolism ; Humans ; Liver Cirrhosis, Experimental/metabolism
Chemical Substances	Adenosine Triphosphate (8L70Q75FXE)
Language	English
Publishing date	2014-08
Publishing country	Netherlands
Document type	Letter ; Comment
ZDB-ID	605953-3
ISSN	1600-0641 ; 0168-8278
ISSN (online)	1600-0641
ISSN	0168-8278
DOI	10.1016/j.jhep.2014.04.017
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Article: Current Management of Alcoholic Hepatitis and Future Therapies.

Saberi, Behnam / Dadabhai, Alia S / Jang, Yoon-Young / Gurakar, Ahmet / Mezey, Esteban

Journal of clinical and translational hepatology

2016 Volume 4, Issue 2, Page(s) 113–122

Abstract: Alcohol is one of the most common etiologies of liver disease, and alcoholic liver disease overall is the second most common indication for liver transplantation in the United States. It encompasses a spectrum of disease, including fatty liver disease, ... ...

Abstract	Alcohol is one of the most common etiologies of liver disease, and alcoholic liver disease overall is the second most common indication for liver transplantation in the United States. It encompasses a spectrum of disease, including fatty liver disease, alcoholic hepatitis (AH), and alcoholic cirrhosis. AH can range from mild to severe disease, with severe disease being defined as: Discriminant Function (DF) ≥ 32, or Model for End-stage Liver Disease (MELD) ≥ 21, or presence of hepatic encephalopathy. Management of the mild disease consists mainly of abstinence and supportive care. Severe AH is associated with significant mortality. Currently, there is no ideal medical treatment for this condition. Besides alcohol cessation, corticosteroids have been used with conflicting results and are associated with an inherent risk of infection. Overall steroids have shown short term benefit when compared to placebo, but they have no obvious long term benefits. Pentoxifylline does not improve survival in patients with severe AH and is no longer recommended based on the results of the STOPAH (Steroid Or Pentoxifylline for Alcoholic Hepatitis) trial. Anti-tumor necrosis factor (TNF) agents are associated with increased risk of life threatening infections and death. Currently, early stage trials are underway, mainly targeting novel pathways based on disease pathogenesis, including modulation of innate immune system, inhibition of gut-liver axis and cell death pathways, and activation of transcription factor farnesyl X receptor (FXR). Future treatment may lie in human induced pluripotent stem cell (iPSC) technology, which is currently under investigation for the study of pathogenesis, drug discovery, and stem cell transplantation. Liver transplantation has been reported with good results in highly selected patients but is controversial due to limited organ supply.
Language	English
Publishing date	2016-06-15
Publishing country	China
Document type	Journal Article ; Review
ZDB-ID	3019822-7
ISSN	2310-8819 ; 2225-0719
ISSN (online)	2310-8819
ISSN	2225-0719
DOI	10.14218/JCTH.2016.00006
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Article ; Online: Acetaldehyde increases endogenous adiponectin and fibrogenesis in hepatic stellate cells but exogenous adiponectin inhibits fibrogenesis.

Potter, James J / Mezey, Esteban

Alcoholism, clinical and experimental research

2007 Volume 31, Issue 12, Page(s) 2092–2100

Abstract: Background: Adiponectin has antifibrogenic properties. Acetaldehyde, the principal metabolite of ethanol, is known to stimulate the expression of type I collagen genes and the production of type I collagen by wild-type (wt) but not by obese gene (ob/ob) ...

Abstract	Background: Adiponectin has antifibrogenic properties. Acetaldehyde, the principal metabolite of ethanol, is known to stimulate the expression of type I collagen genes and the production of type I collagen by wild-type (wt) but not by obese gene (ob/ob) stellate cells. The aim of this study was to determine the expression of adiponectin in activated stellate cells obtained from wt and ob/ob mice and to determine the effects of acetaldehyde on adiponectin in relation to the expression of type I collagen. Methods: Stellate cells were isolated from wt and ob/ob mice by perfusion of the portal vein and cultured. Cell adiponectin was visualized by immunohistochemistry and confocal microscopy and determined by radioimmunoassay and by western blot. Adiponectin mRNA and alpha(1)(I) collagen mRNA were determined by quantitative real time polymerase chain reaction. Results: Adiponectin levels were similar in wt and ob/ob stellate cells. Adiponectin receptor 2 mRNA (AdipoR2 mRNA) and AdipoR2 immunoprotein were higher in ob/ob than in wt stellate cells (p < 0.01). Acetaldehyde (200 microM) increased adiponectin both in wt and in ob/ob stellate cells (p < 0.05), but increased AdipoR2 immunoprotein only in ob/ob stellate cells (p < 0.01). However, in the presence of leptin, acetaldehyde decreased adiponectin in ob/ob stellate cells (p < 0.01). Acetaldehyde enhanced alpha(1)(I) collagen mRNA in wt (p < 0.05), but decreased it in ob/ob stellate cells (p < 0.01). Leptin abrogated the effect of acetaldehyde in decreasing alpha(1)(I) collagen mRNA in ob/ob stellate cells (p < 0.01). Adiponectin inhibited alpha(1)(I) collagen mRNA in the basal state in wt stellate cells or when enhanced by acetaldehyde. Conclusions: Adiponectin and adiponectin receptor are present in activated stellate cells. Adiponectin has a negative regulatory role on the enhancing effect of acetaldehyde on fibrogenesis in alcoholic liver disease.
MeSH term(s)	Acetaldehyde/antagonists & inhibitors ; Acetaldehyde/pharmacology ; Adiponectin/genetics ; Adiponectin/pharmacology ; Animals ; Blotting, Western ; Cells, Cultured ; Collagen Type I/genetics ; Drug Interactions ; Fibrosis/pathology ; Gene Expression/drug effects ; Hepatocytes/drug effects ; Hepatocytes/pathology ; Liver/drug effects ; Liver/pathology ; Liver Cirrhosis/chemically induced ; Liver Cirrhosis/pathology ; Liver Cirrhosis/prevention & control ; Male ; Mice ; Mice, Obese ; Microscopy, Confocal ; Polymerase Chain Reaction ; RNA, Messenger/genetics ; Radioimmunoassay ; Receptors, Adiponectin/drug effects ; Receptors, Adiponectin/genetics
Chemical Substances	Adiponectin ; Collagen Type I ; RNA, Messenger ; Receptors, Adiponectin ; adiponectin receptor 1, mouse ; Acetaldehyde (GO1N1ZPR3B)
Language	English
Publishing date	2007-12
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	428999-7
ISSN	1530-0277 ; 0145-6008
ISSN (online)	1530-0277
ISSN	0145-6008
DOI	10.1111/j.1530-0277.2007.00529.x
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Zs.A 1375: Show issues

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Article ; Online: Elevated mitochondrial activity distinguishes fibrogenic hepatic stellate cells and sensitizes for selective inhibition by mitotropic doxorubicin.

Gajendiran, Priya / Vega, Leonel Iglesias / Itoh, Kie / Sesaki, Hiromi / Vakili, Mohammad Reza / Lavasanifar, Afsaneh / Hong, Kelvin / Mezey, Esteban / Ganapathy-Kanniappan, Shanmugasundaram

Journal of cellular and molecular medicine

2018 Volume 22, Issue 4, Page(s) 2210–2219

Abstract: Activation of hepatic stellate cells (HSCs) is an integral component of the wound-healing process in liver injury/inflammation. However, uncontrolled activation of HSCs leads to constant secretion of collagen-rich extracellular matrix (ECM) proteins, ... ...

Abstract	Activation of hepatic stellate cells (HSCs) is an integral component of the wound-healing process in liver injury/inflammation. However, uncontrolled activation of HSCs leads to constant secretion of collagen-rich extracellular matrix (ECM) proteins, resulting in liver fibrosis. The enhanced ECM synthesis/secretion demands an uninterrupted supply of intracellular energy; however, there is a paucity of data on the bioenergetics, particularly the mitochondrial (mito) metabolism of fibrogenic HSCs. Here, using human and rat HSCs in vitro, we show that the mito-respiration, mito-membrane potential (Δψm) and cellular 'bioenergetic signature' distinguish fibrogenic HSCs from normal, less-active HSCs. Ex vivo, HSCs from mouse and rat models of liver fibrosis further confirmed the altered 'bioenergetic signature' of fibrogenic HSCs. Importantly, the distinctive elevation in mito-Δψm sensitized fibrogenic HSCs for selective inhibition by mitotropic doxorubicin while normal, less-active HSCs and healthy human primary hepatocytes remained minimally affected if not, unaffected. Thus, the increased mito-Δψm may provide an opportunity to selectively target fibrogenic HSCs in liver fibrosis.
MeSH term(s)	Animals ; Cell Line ; Doxorubicin/pharmacology ; Energy Metabolism ; Hepatic Stellate Cells/drug effects ; Hepatic Stellate Cells/metabolism ; Hepatocytes/drug effects ; Hepatocytes/metabolism ; Humans ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology ; Membrane Potential, Mitochondrial/drug effects ; Metabolic Flux Analysis ; Mitochondria, Liver/drug effects ; Mitochondria, Liver/metabolism ; Rats
Chemical Substances	Doxorubicin (80168379AG)
Language	English
Publishing date	2018-02-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2074559-X
ISSN	1582-4934 ; 1582-4934 ; 1582-1838
ISSN (online)	1582-4934
ISSN	1582-4934 ; 1582-1838
DOI	10.1111/jcmm.13501
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Article ; Online: The combination of selenium and vitamin E inhibits type I collagen formation in cultured hepatic stellate cells.

Mezey, Esteban / Liu, Xiaopu / Potter, James J

Biological trace element research

2011 Volume 140, Issue 1, Page(s) 82–94

Abstract: This study investigated the effects of sodium selenite (Se) and of vitamin E (D-α-tochopherol) on the deposition of type I collagen by human LX-2 stellate cells. The cultured cells were treated with or without Se or vitamin E and with or without ... ...

Abstract	This study investigated the effects of sodium selenite (Se) and of vitamin E (D-α-tochopherol) on the deposition of type I collagen by human LX-2 stellate cells. The cultured cells were treated with or without Se or vitamin E and with or without transforming growth factor β1 (TGFβ1). The combination of Se and vitamin E, but not either alone, protected against hepatic fibrosis by decreasing TGFβ1-mediated collagen secretion and accumulation by the stellate cells. This protective effect is due to a combination of decreased formation, decreased stability and increased degradation of the collagen. Effects of Se and vitamin E in decreasing α(1)(I) collagen mRNA and increasing apoptosis of stellate cells indicate decreased formation of collagen, while decreases in transglutaminase 2, which catalyze cross-linking of collagen, lead to decreased stability of the secreted collagen. Effects of Se and vitamin E on reducing tissue inhibitor metalloproteinase 1 (TIMP-1) are associated with increased degradation. The combination of Se and vitamin E decreased lipid peroxidation, while Se alone increased the activity of the antioxidant enzyme thioredoxin reductase. In conclusion, the combination of Se and vitamin E protected against TGFβ1-mediated hepatic fibrosis by decreasing TGFβ1-mediated type I collagen accumulation by stellate cells. This effect is due to a combination of decreased formation, decreased stability and increased degradation of the collagen.
MeSH term(s)	Cells, Cultured ; Collagen Type I/antagonists & inhibitors ; Collagen Type I/biosynthesis ; Hepatic Stellate Cells/cytology ; Hepatic Stellate Cells/drug effects ; Hepatic Stellate Cells/metabolism ; Humans ; Procollagen/antagonists & inhibitors ; Procollagen/biosynthesis ; Sodium Selenite/pharmacology ; Structure-Activity Relationship ; Vitamin E/pharmacology
Chemical Substances	Collagen Type I ; Procollagen ; Vitamin E (1406-18-4) ; Sodium Selenite (HIW548RQ3W)
Language	English
Publishing date	2011-04
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	445336-0
ISSN	1559-0720 ; 0163-4984
ISSN (online)	1559-0720
ISSN	0163-4984
DOI	10.1007/s12011-010-8672-7
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Article: The Combination of Selenium and Vitamin E Inhibits Type I Collagen Formation in Cultured Hepatic Stellate Cells

Mezey, Esteban / Liu, Xiaopu / Potter, James J

Biological trace element research.. 2011 Apr., v. 140, no. 1

2011

Abstract	This study investigated the effects of sodium selenite (Se) and of vitamin E (D-α-tochopherol) on the deposition of type I collagen by human LX-2 stellate cells. The cultured cells were treated with or without Se or vitamin E and with or without transforming growth factor β1 (TGFβ1). The combination of Se and vitamin E, but not either alone, protected against hepatic fibrosis by decreasing TGFβ1-mediated collagen secretion and accumulation by the stellate cells. This protective effect is due to a combination of decreased formation, decreased stability and increased degradation of the collagen. Effects of Se and vitamin E in decreasing α1(I) collagen mRNA and increasing apoptosis of stellate cells indicate decreased formation of collagen, while decreases in transglutaminase 2, which catalyze cross-linking of collagen, lead to decreased stability of the secreted collagen. Effects of Se and vitamin E on reducing tissue inhibitor metalloproteinase 1 (TIMP-1) are associated with increased degradation. The combination of Se and vitamin E decreased lipid peroxidation, while Se alone increased the activity of the antioxidant enzyme thioredoxin reductase. In conclusion, the combination of Se and vitamin E protected against TGFβ1-mediated hepatic fibrosis by decreasing TGFβ1-mediated type I collagen accumulation by stellate cells. This effect is due to a combination of decreased formation, decreased stability and increased degradation of the collagen.
Keywords	antioxidant activity ; apoptosis ; collagen ; crosslinking ; cultured cells ; fibrosis ; humans ; lead ; lipid peroxidation ; messenger RNA ; protective effect ; protein-glutamine gamma-glutamyltransferase ; secretion ; selenium ; sodium selenite ; transforming growth factors ; vitamin E
Language	English
Dates of publication	2011-04
Size	p. 82-94.
Publishing place	Springer-Verlag
Document type	Article
ZDB-ID	445336-0
ISSN	1559-0720 ; 0163-4984
ISSN (online)	1559-0720
ISSN	0163-4984
DOI	10.1007/s12011-010-8672-7
Database	NAL-Catalogue (AGRICOLA)

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