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1. Author Correction: Defective HNF4alpha-dependent gene expression as a driver of hepatocellular failure in alcoholic hepatitis

Author

Argemi, Josepmaria, Latasa, Maria U., Atkinson, Stephen R., Blokhin, Ilya O., Massey, Veronica, Gue, Joel P., Cabezas, Joaquin, Lozano, Juan J., Van Booven, Derek, Bell, Aaron, Cao, Sheng, Vernetti, Lawrence A., Arab, Juan P., Ventura-Cots, Meritxell, Edmunds, Lia R., Fondevila, Constantino, Stärkel, Peter, Dubuquoy, Laurent, Louvet, Alexandre, Odena, Gemma, Gomez, Juan L., Aragon, Tomas, Altamirano, Jose, Caballeria, Juan, Jurczak, Michael J., Taylor, D. Lansing, Berasain, Carmen, Wahlestedt, Claes, Monga, Satdarshan P., Morgan, Marsha Y., Sancho-Bru, Pau, Mathurin, Philippe, Furuya, Shinji, Lackner, Carolin, Rusyn, Ivan, Shah, Vijay H., Thursz, Mark R., Mann, Jelena, Avila, Matias A., and Bataller, Ramon

Published
2023
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2. Selonsertib for patients with bridging fibrosis or compensated cirrhosis due to NASH: Results from randomized phase III STELLAR trials

Author

Gadano, Adrian, Martins, Marcelo, Angus, Peter, Bate, John, Danta, Mark, George, Jacob, Hodge, Alexander, Kontorinis, Nickolas, Roberts, Stuart, Sanagapalli, Santosh, Skoien, Richard, Thompson, Alexander, Zekry, Amany, Stauber, Rudolf, Trauner, Michael, Moreno, Christophe, Reynaert, Hendrik, Verbeke, Len, Silva, Mario Reis Alvares da, Parise, Edison, Oliveira, Claudia Pinto Marques Souza de, Araujo, Roberta Chaves, Martinelli, Ana de Lourdes Candolo, Borman, Meredith, Chandok, Natasha, Elkhashab, Magdy, Fraser, Hughie, Kaita, Kelly, Ma, Mang, Marotta, Paul, Ramji, Alnoor, Tam, Edward, Yoshida, Eric, Swain, Mark, Sebastiani, Giada, Petrunia, Denis, Abergel, Armando, Anty, Rodolphe, Bourlière, Marc, Boursier, Jérôme, Bureau, Christophe, Castera, Laurent, Habersetzer, François, Hézode, Christophe, Ledinghen, Victor De, Leroy, Vincent, Loustaud-Ratti, Véronique, Mathurin, Philippe, Pol, Stanislas, Zoulim, Fabien, Hinrichsen, Holger, Ingiliz, Patrick, Lammert, Frank, Manns, Michael, Schattenberg, Jörn, Schiefke, Ingolf, Trautwein, Christian, Zeuzem, Stefan, Hui, Aric, Li, King-Kong, Wong, Vincent, Acharya, Subrat, Chowdhury, Abhijit, Duseja, Ajay, Kapoor, Dharmesh, Mukewar, Shrikant, Sarin, Shiv, Shah, Samir, Shalimar, Sood, Ajit, Tantry, BV, Ben-Ari, Ziv, Katchman, Helena, Safadi, Rifaat, Veitsman, Ella, Zuckerman, Eli, Brunetto, Maurizia, Lampertico, Pietro, Mangia, Alessandra, Akahane, Takemi, Akuta, Norio, Eguchi, Yuichiro, Fujiyama, Shigetoshi, Genda, Takuya, Hiasa, Yoichi, Ido, Akio, Ikeda, Fusao, Ikegami, Tadashi, Imajo, Kento, Itoh, Yoshito, Iwasa, Motoh, Karino, Yoshiyasu, Kato, Naoya, Kawaguchi, Takumi, Kawanaka, Miwa, Kido, Masahiro, Kobayashi, Tomoo, Kurosaki, Masayuki, Matsuzaki, Yasushi, Mita, Eiji, Mizukoshi, Eishiro, Nakahara, Takashi, Nomura, Hideyuki, Notsumata, Kazuo, Okanoue, Takeshi, Saito, Satoshi, Sakugawa, Hiroshi, Suzuki, Yoshiyuki, Takaguchi, Koichi, Takaki, Akinobu, Takashima, Tomoyuki, Tanaka, Saiyu, Tsuji, Keiji, Ueno, Yoshiyuki, Umemura, Takeji, Uto, Hirofumi, Yamashita, Nobuyuki, Yanase, Mikio, Yatsuhashi, Hiroshi, Yoneda, Masashi, Chan, Wah Kheong, Tan, Soek Siam, Garza, Laura Cisneros, Ladron De Guevara Cetina, Alma, Angeles, Rocio Guadalupe Vargas, Silva, Francisca Martinez, Van Erpecum, Karel, Orr, David, Jabłkowski, Maciej, Jaroszewicz, Jerzy, Ramos, Jose, Ahmed, Taufique, Ang, Tiing, Dan, Yock young, Goh, Boon Bee, Kaliyaperumal, Kalaiyarasi, Yip, Cherng Hann, Baik, Soon Koo, Jang, Byoung Kuk, Jun, Dae Won, Kim, Won, Kim, Hyung Joon, Kim, Ji Hoon, Lee, Kwan Sik, Lee, Chun Kyon, Lim, Young-Suk, Park, Jun Yong, Tak, Won Young, Augustin, Salvador, Perez, Salvador Benlloch, Caballeria, Juan, Luis, Jose, Panero, Calleja, Rodríguez, Jose Carrión, Garcia, Javier Crespo, Samaniego, Javier Garcia, Gibert, Pere Ginès, Prieto, Martin, Gomez, Manuel Romero, Turnes, Juan, Dufour, Jean-Francois, Moriggia, Alberto, Sheen, I-Shyan, Kao, Jia-Horng, Cheng, Pin-Nan, Huang, Jee-Fu, Yang, Sheng-Shun, Su, Wei-Wen, Chen, Chi-Yi, Chien, Rong-Nan, Lo, Gin-Ho, Chu, Chi-Jen, Wang, Horng-Yuan, Hu, Jui-Ting, Huang, Yi Wen, Agarwal, Kosh, Allison, Michael, Anstee, Quentin, Austin, Andrew, Fowell, Andrew, Ch'ng, Chin Lye, Manousou, Pinelopi, Newsome, Philip, Ryder, Stephen, Shankar, Arun, Abdelmalek, Manal, Abrams, Gary, Aguilar, Humberto, Alam, Imtiaz, Alba, Laura, Alkhouri, Naim, Allen, Alina, Aqel, Bashar, Balart, Luis, Barritt, A. Sidney, IV, Behari, Jaideep, Bennett, Michael, Bernstein, David, Bhandari, Bal Raj, Bonacini, Maurizio, Borg, Brian, Brown, Kimberly, Bzowej, Natalie, Caldwell, Stephen, Chami, Tawfik, Coates, Allan, Cueli, Adolfo, Davis, Mitchell, deLemos, Andrew, Desai, Archita, Dunn, Winston, Ferreira, Nelson, Fine, Michael, Firpi-Morell, Roberto, Freedland, Curtis, Freilich, Bradley, Fuchs, Michael, Galambos, Michael, Gallegos-Orozco, Juan, Galler, Greg, Ghali, Maged, Ghalib, Reem, Gill, Satinder, Gillis, Marcum, Gilroy, Richard, Gordon, Stuart, Gunn, Nadege, Halegoua-DeMarzio, Dina, Hassan, Mohamed, Hassanein, Tarek, Herring, Robert, Jr., Hong, John, Huang, Jonathan, Kabler, Heidi, Kayali, Zeid, Knapple, Whitfield, Kolli, Geetha, Kowdley, Kris, Krause, Richard, Lawitz, Eric, Lidofsky, Steven, Lim, Joseph, Lipkis, Donald, Loomba, Rohit, Mahgoub, Amar, Malespin, Miguel, Manch, Richard, Mannis, Steven, Manos, Paul, McDonald, Thomas, McKenzie, Mark, Mena, Edward, Merriman, Raphael, Moehlen, Martin William, Montgomery, Richard, Murphy, Robert, Natarajan, Yamini, Neff, Guy, Noureddin, Mazen, Ortiz-Lasanta, Grisell, Pagadala, Mangesh, Patel, Keyur, Patton, Heather, Peyton, Adam, Pimstone, Neville, Poulos, John, Pound, David, Pyrsopoulos, Nikolaos, Rafiq, Nila, Ravendhran, Natarajan, Ravinuthala, Ravi, Reddy, K. Rajendar, Reindollar, Robert, Reynolds, Justin, Rinella, Mary, Rizvi, Syed, Rockey, Don, Rodriguez-Perez, Federico, Ruane, Peter, Rubin, Raymond, Ryan, Michael, Saeian, Kia, Sanyal, Arun, Sarkar, Souvik, Scanga, Andrew, Schiff, Eugene, Schmidt, Warren, Schneider, Jeffrey, Sepe, Thomas, Shah, Dhiren, Shaikh, Obaid, Shankar, Uday, Sheikh, Aasim, Sheikh, Muhammad, Sherman, Kenneth, Shiffman, Mitchell, Siddique, Asma, Smith, Matthew, Suarez, Rosa, Talal, Andrew, Te, Helen, Tekola, Bezawit, Tetri, Brent, Thuluvath, Paul, Toro, Doris, Torres, Dawn, Trinh, Huy, Trotter, James, Vento, Angel, Vierling, John, Vuppalanchi, Raj, Waters, Michael, Weisberg, Ilan, Wieland, Amanda, Williams, Alonzo, Younes, Ziad, Adams, Leon, Harding, Damian, Hodge, Alex, Kontorinis, Nick, Strasser, Simone, Thompson, Alex, Horsmans, Yves, Steenkiste, Christophe Van, Bailey, Robert, Giard, Jeanne-Marie, Montano-Loza, Aldo, Puglia, Marco, Tsoi, Keith, Larrey, Dominique, Nguyen-Khac, Eric, Ratziu, Vlad, Spengler, Ulrich, Wiegand, Johannes, Hui, Aric Josun, Acharya, Subrat Kumar, Sarin, Shiv Kumar, Tantry, Vishwanath, Braun, Marius, Hazzan, Rawi, Lurie, Yoav, Colombo, Massimo, Fujii, Hideki, Hashimoto, Etsuko, Kato, Masaki, Ogawa, Koji, Takehara, Tetsuo, Tokushige, Katsutoshi, Garza, Laura Esthela Cisneros, Ladrón De Guevara, Alma Laura, Schultz, Michael, Janczewska, Ewa, Toro, Doris H., Jeong, Sook-Hyang, Kim, Yoon Jun, Lee, Jin-Woo, Ang, Tiing Leong, Bee, George Goh Boon, Benlloch, Salvador, Caballería, Juan, Calleja, José Luis, Rodríguez, Jose A. Carrión, Crespo, Javier, Diago, Moises, Fernandez-Rodriguez, Conrado, García-Samaniego, Javier, Ginès, Pere, Romero, Manuel, Dufour, Jean-François, Alazawi, William, Ch'ng, Chin-Lye, Forton, Daniel, Priest, Matthew, Sheridan, David, Ankoma-Sey, Victor, Balakrishnan, Maya, Bambha, Kiran, Barritt, A. Sidney, Bhandari, Bal, Brandman, Danielle, Chang, Charissa, Corey, Kathleen, Feldman, Michael, Gholam, Pierre, Goff, John, Marzio, Dina Halegoua-De, Harrison, Stephen, Hellstern, Paul, Jr., Herring, Robert, Iyer, Rajalakshmi, Jakiche, Antoine, Kohli, Anita, Krok, Karen, Kugelmas, Marcelo, Kumar, Sonal, Lai, Michelle, Mahmoud, Mitchell, Mantry, Parvez, Marsano, Luis, Nguyen, Tuan, Park, James, Patton, Heather M., Pockros, Paul, Reddy, Rajender, Rodriguez, Miguel, Sarles, Harry, Satapathy, Sanjaya, Sedghi, Shahriar, Shah, Nikunj, Sheikh, Muhammad Yasin, Sigal, Samuel, Stanca, Carmen, Steinbook, Michael, Szabo, Gyongyi, Terrault, Norah, Tong, Myron, Victor, David, Zervos, Xaralambos, Harrison, Stephen A., Wong, Vincent Wai-Sun, Caldwell, Stephen H., Shiffman, Mitchell L., Camargo, Marianne, Li, Georgia, Kersey, Kathryn, Jia, Catherine, Zhu, Yanni, Djedjos, C. Stephen, Subramanian, G. Mani, Myers, Robert P., Anstee, Quentin M., Romero-Gomez, Manuel, Goodman, Zachary, Lawitz, Eric J., and Younossi, Zobair

Published
2020
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3. A randomized, placebo‐controlled trial of cenicriviroc for treatment of nonalcoholic steatohepatitis with fibrosis

Author

Friedman, Scott L, Ratziu, Vlad, Harrison, Stephen A, Abdelmalek, Manal F, Aithal, Guruprasad P, Caballeria, Juan, Francque, Sven, Farrell, Geoffrey, Kowdley, Kris V, Craxi, Antonio, Simon, Krzysztof, Fischer, Laurent, Melchor‐Khan, Liza, Vest, Jeffrey, Wiens, Brian L, Vig, Pamela, Seyedkazemi, Star, Goodman, Zachary, Wong, Vincent Wai‐Sun, Loomba, Rohit, Tacke, Frank, Sanyal, Arun, and Lefebvre, Eric

Subjects
Hepatitis, Patient Safety, Clinical Research, Chronic Liver Disease and Cirrhosis, Liver Disease, Clinical Trials and Supportive Activities, Digestive Diseases, 6.1 Pharmaceuticals, Evaluation of treatments and therapeutic interventions, Oral and gastrointestinal, Adult, Aged, Biomarkers, CCR5 Receptor Antagonists, Double-Blind Method, Female, Humans, Imidazoles, Liver, Liver Cirrhosis, Male, Middle Aged, Non-alcoholic Fatty Liver Disease, Sulfoxides, Treatment Outcome, Medical Biochemistry and Metabolomics, Clinical Sciences, Immunology, Gastroenterology & Hepatology
Abstract

The aim of this study was to evaluate cenicriviroc (CVC), a dual antagonist of CC chemokine receptor types 2 and 5, for treatment of nonalcoholic steatohepatitis (NASH) with liver fibrosis (LF). A randomized, double-blind, multinational phase 2b study enrolled subjects with NASH, a nonalcoholic fatty liver disease activity score (NAS) ≥4, and LF (stages 1-3, NASH Clinical Research Network) at 81 clinical sites. Subjects (N = 289) were randomly assigned CVC 150 mg or placebo. Primary outcome was ≥2-point improvement in NAS and no worsening of fibrosis at year 1. Key secondary outcomes were: resolution of steatohepatitis (SH) and no worsening of fibrosis; improvement in fibrosis by ≥1 stage and no worsening of SH. Biomarkers of inflammation and adverse events were assessed. Full study recruitment was achieved. The primary endpoint of NAS improvement in the intent-to-treat population and resolution of SH was achieved in a similar proportion of subjects on CVC (N = 145) and placebo (N = 144; 16% vs. 19%, P = 0.52 and 8% vs. 6%, P = 0.49, respectively). However, the fibrosis endpoint was met in significantly more subjects on CVC than placebo (20% vs. 10%; P = 0.02). Treatment benefits were greater in those with higher disease activity and fibrosis stage at baseline. Biomarkers of systemic inflammation were reduced with CVC. Safety and tolerability of CVC were comparable to placebo.ConclusionAfter 1 year of CVC treatment, twice as many subjects achieved improvement in fibrosis and no worsening of SH compared with placebo. Given the urgent need to develop antifibrotic therapies in NASH, these findings warrant phase 3 evaluation. (Hepatology 2018;67:1754-1767).

Published
2018

4. Deregulated neddylation in liver fibrosis

Author

Zubiete‐Franco, Imanol, Fernández‐Tussy, Pablo, Barbier‐Torres, Lucía, Simon, Jorge, Fernández‐Ramos, David, Lopitz‐Otsoa, Fernando, Juan, Virginia Gutiérrez‐de, de Davalillo, Sergio López, Duce, Antonio Martín, Iruzubieta, Paula, Taibo, Daniel, Crespo, Javier, Caballeria, Juan, Villa, Erica, Aurrekoetxea, Igor, Aspichueta, Patricia, Varela‐Rey, Marta, Lu, Shelly C, Mato, José M, Beraza, Naiara, Delgado, Teresa C, and Martínez‐Chantar, María L

Subjects
Digestive Diseases, Chronic Liver Disease and Cirrhosis, Liver Disease, 2.1 Biological and endogenous factors, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Aetiology, Oral and gastrointestinal, Good Health and Well Being, Aging, Analysis of Variance, Animals, Apoptosis, Biopsy, Needle, Cell Proliferation, Cell Survival, Cells, Cultured, Chemokine CCL4, Chemokines, Cyclopentanes, Disease Models, Animal, Hepatic Stellate Cells, Humans, Immunohistochemistry, Liver Cirrhosis, Male, Mice, Mice, Inbred C57BL, NEDD8 Protein, Pyrimidines, Random Allocation, Signal Transduction, Ubiquitins, Medical Biochemistry and Metabolomics, Clinical Sciences, Immunology, Gastroenterology & Hepatology
Abstract

Hepatic fibrosis is a global health problem currently without effective therapeutic approaches. Even though the ubiquitin-like posttranslational modification of neddylation, that conjugates Nedd8 (neural precursor cell expressed developmentally downregulated) to specific targets, is aberrant in many pathologies, its relevance in liver fibrosis (LF) remained unexplored. Our results show deregulated neddylation in clinical fibrosis and both in mouse bileductligation- and CCl4 -induced fibrosis. Importantly, neddylation inhibition, by using the pharmacological inhibitor, MLN4924, reduced liver injury, apoptosis, inflammation, and fibrosis by targeting different hepatic cell types. On one hand, increased neddylation was associated with augmented caspase 3 activity in bile-acid-induced apoptosis in mouse hepatocytes whereas neddylation inhibition ameliorated apoptosis through reduction of expression of the Cxcl1 and Ccl2 chemokines. On the other hand, chemokine receptors and cytokines, usually induced in activated macrophages, were reduced after neddylation inhibition in mouse Kupffer cells. Under these circumstances, decreased hepatocyte cell death and inflammation after neddylation inhibition could partly account for reduction of hepatic stellate cell (HSC) activation. We provide evidence that augmented neddylation characterizes activated HSCs, suggesting that neddylation inhibition could be important for resolving LF by directly targeting these fibrogenic cells. Indeed, neddylation inhibition in activated HSCs induces apoptosis in a process partly mediated by accumulation of c-Jun, whose cullin-mediated degradation is impaired under these circumstances.ConclusionNeddylation inhibition reduces fibrosis, suggesting neddylation as a potential and attractive therapeutic target in liver fibrosis. (Hepatology 2017;65:694-709).

Published
2017

5. LPS-TLR4 Pathway Mediates Ductular Cell Expansion in Alcoholic Hepatitis.

Author

Odena, Gemma, Chen, Jiegen, Lozano, Juan Jose, Altamirano, Jose, Rodrigo-Torres, Daniel, Affo, Silvia, Morales-Ibanez, Oriol, Matsushita, Hiroshi, Zou, Jian, Dumitru, Raluca, Caballeria, Juan, Gines, Pere, Arroyo, Vicente, You, Min, Rautou, Pierre-Emmanuel, Valla, Dominique, Crews, Fulton, Seki, Ekihiro, Sancho-Bru, Pau, and Bataller, Ramon

Subjects
Hepatic Duct, Common, Cells, Cultured, Hepatocytes, Animals, Mice, Inbred BALB C, Mice, Knockout, Humans, Mice, Hepatitis, Alcoholic, Collagen, Lipopolysaccharides, Gene Expression Profiling, Signal Transduction, Cell Proliferation, Gene Expression Regulation, Middle Aged, Female, Male, Toll-Like Receptor 4, Keratins, Type I, Biotechnology, Substance Abuse, Hepatitis, Alcoholism, Alcohol Use and Health, Digestive Diseases, Liver Disease, Chronic Liver Disease and Cirrhosis, 2.1 Biological and endogenous factors, 1.1 Normal biological development and functioning, Oral and Gastrointestinal, Hepatic Duct, Common, Cells, Cultured, Inbred BALB C, Knockout, Alcoholic, Keratins, Type I, Biochemistry and Cell Biology, Other Physical Sciences
Abstract

Alcoholic hepatitis (AH) is the most severe form of alcoholic liver disease for which there are no effective therapies. Patients with AH show impaired hepatocyte proliferation, expansion of inefficient ductular cells and high lipopolysaccharide (LPS) levels. It is unknown whether LPS mediates ductular cell expansion. We performed transcriptome studies and identified keratin 23 (KRT23) as a new ductular cell marker. KRT23 expression correlated with mortality and LPS serum levels. LPS-TLR4 pathway role in ductular cell expansion was assessed in human and mouse progenitor cells, liver slices and liver injured TLR4 KO mice. In AH patients, ductular cell expansion correlated with portal hypertension and collagen expression. Functional studies in ductular cells showed that KRT23 regulates collagen expression. These results support a role for LPS-TLR4 pathway in promoting ductular reaction in AH. Maneuvers aimed at decreasing LPS serum levels in AH patients could have beneficial effects by preventing ductular reaction development.

Published
2016

6. Enfermedad hepática por alcohol. Guías de práctica clínica. Documento de consenso auspiciado por la AEEH

Author

Bataller, Ramón, Cabezas, Joaquín, Aller, Rocío, Ventura-Cots, Meritxell, Abad, Javier, Albillos, Agustín, Altamirano, José, Arias-Loste, María Teresa, Bañares, Rafael, Caballería, Juan, Caballería, Llorenç, Carrión, José Antonio, Diago, Moisés, Fernández Rodríguez, Conrado, Gallego, Rocío, García-Cortes, Miren, García-Monzón, Carmelo, Genescà, Joan, Ginés, Pere, Hernandez-Guerra, Manuel, Jorquera, Francisco, Lligoña, Anna, Molina, Esther, Pareja, María Jesús, Planas, Ramón, Tomé, Santiago, Salmerón, Javier, and Romero-Gómez, Manuel

Published
2019
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8. Dysregulation of serum bile acids and FGF19 in alcoholic hepatitis

Author

Brandl, Katharina, Hartmann, Phillipp, Jih, Lily J., Pizzo, Donald P., Argemi, Josepmaria, Ventura-Cots, Meritxell, Coulter, Sally, Liddle, Christopher, Ling, Lei, Rossi, Stephen J., DePaoli, Alex M., Loomba, Rohit, Mehal, Wajahat Z., Fouts, Derrick E., Lucey, Michael R., Bosques-Padilla, Francisco, Mathurin, Philippe, Louvet, Alexander, Garcia-Tsao, Guadalupe, Verna, Elizabeth C., Abraldes, Juan G., Brown, Robert S., Jr, Vargas, Victor, Altamirano, Jose, Caballería, Juan, Shawcross, Debbie, Stärkel, Peter, Ho, Samuel B., Bataller, Ramon, and Schnabl, Bernd

Published
2018
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9. High Prevalence of Liver Fibrosis Among European Adults With Unknown Liver Disease: A Population-Based Study

Author

Caballería, Llorenç, Pera, Guillem, Arteaga, Ingrid, Rodríguez, Lluís, Alumà, Alba, Morillas, Rosa M<ce:sup loc='post">a</ce:sup>, de la Ossa, Napoleón, Díaz, Alba, Expósito, Carmen, Miranda, Dolores, Sánchez, Carmen, Prats, Rosa M<ce:sup loc='post">a</ce:sup>, Urquizu, Marta, Salgado, Angels, Alemany, Magda, Martinez, Alba, Majeed, Irfan, Fabrellas, Núria, Graupera, Isabel, Planas, Ramón, Ojanguren, Isabel, Serra, Miquel, Torán, Pere, Caballería, Juan, and Ginès, Pere

Published
2018
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11. Defective HNF4alpha-dependent gene expression as a driver of hepatocellular failure in alcoholic hepatitis

Author

Argemi, Josepmaria, Latasa, Maria U., Atkinson, Stephen R., Blokhin, Ilya O., Massey, Veronica, Gue, Joel P., Cabezas, Joaquin, Lozano, Juan J., Van Booven, Derek, Bell, Aaron, Cao, Sheng, Vernetti, Lawrence A., Arab, Juan P., Ventura-Cots, Meritxell, Edmunds, Lia R., Fondevila, Constantino, Stärkel, Peter, Dubuquoy, Laurent, Louvet, Alexandre, Odena, Gemma, Gomez, Juan L., Aragon, Tomas, Altamirano, Jose, Caballeria, Juan, Jurczak, Michael J., Taylor, D. Lansing, Berasain, Carmen, Wahlestedt, Claes, Monga, Satdarshan P., Morgan, Marsha Y., Sancho-Bru, Pau, Mathurin, Philippe, Furuya, Shinji, Lackner, Carolin, Rusyn, Ivan, Shah, Vijay H., Thursz, Mark R., Mann, Jelena, Avila, Matias A., and Bataller, Ramon

Published
2019
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13. Clinical, histological and molecular profiling of different stages of alcohol-related liver disease.

Author

UCL - (SLuc) Service de gastro-entérologie, UCL - SSS/IREC/GAEN - Pôle d'Hépato-gastro-entérologie, Ventura-Cots, Meritxell, Argemi, Josepmaria, Jones, Patricia D, Lackner, Carolin, El Hag, Mohamed, Abraldes, Juan G, Alvarado, Edilmar, Clemente, Ana, Ravi, Samitha, Alves, Antonio, Alboraie, Mohamed, Altamirano, Jose, Barace, Sergio, Bosques, Francisco, Brown, Robert, Caballeria, Juan, Cabezas, Joaquin, Carvalhana, Sofia, Cortez-Pinto, Helena, Costa, Adilia, Degré, Delphine, Fernandez-Carillo, Carlos, Ganne-Carrie, Nathalie, Garcia-Tsao, Guadalupe, Genesca, Joan, Koskinas, John, Lanthier, Nicolas, Louvet, Alexandre, Lozano, Juan José, Lucey, Michael R, Masson, Steven, Mathurin, Philippe, Mendez-Sanchez, Nahum, Miquel, Rosa, Moreno, Christophe, Mounajjed, Taofic, Odena, Gemma, Kim, Won, Sancho-Bru, Pau, Warren Sands, R, Szafranska, Justyna, Verset, Laurine, Schnabl, Bern, Sempoux, Christine, Shah, Vijay, Shawcross, Debbie Lindsay, Stauber, Rudolf E, Straub, Beate K, Verna, Elizabeth, Tiniakos, Dina, Trépo, Eric, Vargas, Victor, Villanueva, Càndid, Woosley, John T, Ziol, Marianne, Mueller, Sebastian, Starkel, Peter, Bataller, Ramon, UCL - (SLuc) Service de gastro-entérologie, UCL - SSS/IREC/GAEN - Pôle d'Hépato-gastro-entérologie, Ventura-Cots, Meritxell, Argemi, Josepmaria, Jones, Patricia D, Lackner, Carolin, El Hag, Mohamed, Abraldes, Juan G, Alvarado, Edilmar, Clemente, Ana, Ravi, Samitha, Alves, Antonio, Alboraie, Mohamed, Altamirano, Jose, Barace, Sergio, Bosques, Francisco, Brown, Robert, Caballeria, Juan, Cabezas, Joaquin, Carvalhana, Sofia, Cortez-Pinto, Helena, Costa, Adilia, Degré, Delphine, Fernandez-Carillo, Carlos, Ganne-Carrie, Nathalie, Garcia-Tsao, Guadalupe, Genesca, Joan, Koskinas, John, Lanthier, Nicolas, Louvet, Alexandre, Lozano, Juan José, Lucey, Michael R, Masson, Steven, Mathurin, Philippe, Mendez-Sanchez, Nahum, Miquel, Rosa, Moreno, Christophe, Mounajjed, Taofic, Odena, Gemma, Kim, Won, Sancho-Bru, Pau, Warren Sands, R, Szafranska, Justyna, Verset, Laurine, Schnabl, Bern, Sempoux, Christine, Shah, Vijay, Shawcross, Debbie Lindsay, Stauber, Rudolf E, Straub, Beate K, Verna, Elizabeth, Tiniakos, Dina, Trépo, Eric, Vargas, Victor, Villanueva, Càndid, Woosley, John T, Ziol, Marianne, Mueller, Sebastian, Starkel, Peter, and Bataller, Ramon

Abstract

Alcohol-related liver disease (ALD) ranges from never-decompensated ALD (ndALD) to the life-threatening decompensated phenotype, known as alcohol-related hepatitis (AH). A multidimensional study of the clinical, histological and molecular features of these subtypes is lacking. Two large cohorts of patients were recruited in an international, observational multicentre study: a retrospective cohort of patients with ndALD (n=110) and a prospective cohort of patients with AH (n=225). Clinical, analytical, immunohistochemistry and hepatic RNA microarray analysis of both disease phenotypes were performed. Age and mean alcohol intake were similar in both groups. AH patients had greater aspartate amino transferase/alanine amino transferase ratio and lower gamma-glutamyl transferase levels than in ndALD patients. Patients with AH demonstrated profound liver failure and increased mortality. One-year mortality was 10% in ndALD and 50% in AH. Histologically, steatosis grade, ballooning and pericellular fibrosis were similar in both groups, while advanced fibrosis, Mallory-Denk bodies, bilirubinostasis, severe neutrophil infiltration and ductular reaction were more frequent among AH patients. Transcriptome analysis revealed a profound gene dysregulation within both phenotypes when compare to controls. While ndALD was characterised by deregulated expression of genes involved in matrisome and immune response, the development of AH resulted in a marked deregulation of genes involved in hepatocyte reprogramming and bile acid metabolism. Despite comparable alcohol intake, AH patients presented with worse liver function compared with ndALD patients. Bilirubinostasis, severe fibrosis and ductular reaction were prominent features of AH. AH patients exhibited a more profound deregulation of gene expression compared with ndALD patients.

Published
2022

14. Clinical, histological and molecular profiling of different stages of alcohol-related liver disease.

Author

Ventura-Cots, Meritxell, Argemi, Josepmaria, Jones, Patricia D, Lackner, Carolin, El Hag, Mohamed, Abraldes, Juan G, Alvarado, Edilmar, Clemente, Ana, Ravi, Samhita, Alves, Antonio, Alboraie, Mohamed, Altamirano, Jose, Barace, Sergio, Bosques, Francisco, Brown, Robert, Caballeria, Juan, Cabezas, Joaquin, Carvalhana, Sofia, Cortez-Pinto, Helena, Costa, Adilia, Degré, Delphine, Fernandez-Carrillo, Carlos, Ganne-Carrie, Nathalie, Garcia-Tsao, Guadalupe, Genesca, Joan, Koskinas, John, Lanthier, Nicolas, Louvet, Alexandre, Lozano, Juan José, Lucey, Michael R, Masson, Steven, Mathurin, Philippe, Mendez-Sanchez, Nahum, Miquel, Rosa, Moreno, Christophe, Mounajjed, Taofic, Odena, Gemma, Kim, Won, Sancho-Bru, Pau, Warren Sands, R, Szafranska, Justyna, Verset, Laurine, Schnabl, Bernd, Sempoux, Christine, Shah, Vijay H, Shawcross, Debbie Lindsay, Stauber, Rudolf, Straub, Beate K, Verna, Elizabeth, Tiniakos, Dina, Trepo, Eric, Vargas, Victor, Villanueva, Cándido, Woosley, John T, Ziol, Marianne, Mueller, Sebastian, Stärkel, Peter, Bataller, Ramon, Ventura-Cots, Meritxell, Argemi, Josepmaria, Jones, Patricia D, Lackner, Carolin, El Hag, Mohamed, Abraldes, Juan G, Alvarado, Edilmar, Clemente, Ana, Ravi, Samhita, Alves, Antonio, Alboraie, Mohamed, Altamirano, Jose, Barace, Sergio, Bosques, Francisco, Brown, Robert, Caballeria, Juan, Cabezas, Joaquin, Carvalhana, Sofia, Cortez-Pinto, Helena, Costa, Adilia, Degré, Delphine, Fernandez-Carrillo, Carlos, Ganne-Carrie, Nathalie, Garcia-Tsao, Guadalupe, Genesca, Joan, Koskinas, John, Lanthier, Nicolas, Louvet, Alexandre, Lozano, Juan José, Lucey, Michael R, Masson, Steven, Mathurin, Philippe, Mendez-Sanchez, Nahum, Miquel, Rosa, Moreno, Christophe, Mounajjed, Taofic, Odena, Gemma, Kim, Won, Sancho-Bru, Pau, Warren Sands, R, Szafranska, Justyna, Verset, Laurine, Schnabl, Bernd, Sempoux, Christine, Shah, Vijay H, Shawcross, Debbie Lindsay, Stauber, Rudolf, Straub, Beate K, Verna, Elizabeth, Tiniakos, Dina, Trepo, Eric, Vargas, Victor, Villanueva, Cándido, Woosley, John T, Ziol, Marianne, Mueller, Sebastian, Stärkel, Peter, and Bataller, Ramon

Abstract

Alcohol-related liver disease (ALD) ranges from never-decompensated ALD (ndALD) to the life-threatening decompensated phenotype, known as alcohol-related hepatitis (AH). A multidimensional study of the clinical, histological and molecular features of these subtypes is lacking., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2022

17. Clinical, histological and molecular profiling of different stages of alcohol-related liver disease

Author

Ventura-Cots, Meritxell, primary, Argemi, Josepmaria, additional, Jones, Patricia D, additional, Lackner, Carolin, additional, El Hag, Mohamed, additional, Abraldes, Juan G, additional, Alvarado, Edilmar, additional, Clemente, Ana, additional, Ravi, Samhita, additional, Alves, Antonio, additional, Alboraie, Mohamed, additional, Altamirano, Jose, additional, Barace, Sergio, additional, Bosques, Francisco, additional, Brown, Robert, additional, Caballeria, Juan, additional, Cabezas, Joaquin, additional, Carvalhana, Sofia, additional, Cortez-Pinto, Helena, additional, Costa, Adilia, additional, Degré, Delphine, additional, Fernandez-Carrillo, Carlos, additional, Ganne-Carrie, Nathalie, additional, Garcia-Tsao, Guadalupe, additional, Genesca, Joan, additional, Koskinas, John, additional, Lanthier, Nicolas, additional, Louvet, Alexandre, additional, Lozano, Juan José, additional, Lucey, Michael R, additional, Masson, Steven, additional, Mathurin, Philippe, additional, Mendez-Sanchez, Nahum, additional, Miquel, Rosa, additional, Moreno, Christophe, additional, Mounajjed, Taofic, additional, Odena, Gemma, additional, Kim, Won, additional, Sancho-Bru, Pau, additional, Warren Sands, R, additional, Szafranska, Justyna, additional, Verset, Laurine, additional, Schnabl, Bern, additional, Sempoux, Christine, additional, Shah, Vijay, additional, Shawcross, Debbie Lindsay, additional, Stauber, Rudolf E, additional, Straub, Beate K, additional, Verna, Elizabeth, additional, Tiniakos, Dina, additional, Trépo, Eric, additional, Vargas, Victor, additional, Villanueva, Càndid, additional, Woosley, John T, additional, Ziol, Marianne, additional, Mueller, Sebastian, additional, Stärkel, Peter, additional, and Bataller, Ramon, additional

Published
2022
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19. HuR/Methyl-HuR and AUF1 Regulate the MAT Expressed During Liver Proliferation, Differentiation, and Carcinogenesis

Author

Vázquez–Chantada, Mercedes, Fernández–Ramos, David, Embade, Nieves, Martínez–Lopez, Nuria, Varela–Rey, Marta, Woodhoo, Ashwin, Luka, Zigmund, Wagner, Conrad, Anglim, Paul P., Finnell, Richard H., Caballería, Juan, Laird–Offringa, Ite A., Gorospe, Myriam, Lu, Shelly C., Mato, José M., and Martínez–Chantar, M. Luz

Published
2010
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21. Exogenous Liposomal Ceramide-C6 Ameliorates Lipidomic Profile, Energy Homeostasis, and Anti-Oxidant Systems in NASH

Author

Zanieri, Francesca, Levi, Ana, Montefusco, David, Longato, Lisa, De Chiara, Francesco, Frenguelli, Luca, Omenetti, Sara, Andreola, Fausto, Luong, Tu Vinh, Massey, Veronica, Caballeria, Juan, Fondevila, Constantino, Shanmugavelandy, Sriram S, Fox, Todd, Mazza, Giuseppe, Argemi, Josepmaria, Bataller, Ramon, Cowart, Lauren Ashley, Kester, Mark, Pinzani, Massimo, Rombouts, Krista, Zanieri, Francesca, Levi, Ana, Montefusco, David, Longato, Lisa, De Chiara, Francesco, Frenguelli, Luca, Omenetti, Sara, Andreola, Fausto, Luong, Tu Vinh, Massey, Veronica, Caballeria, Juan, Fondevila, Constantino, Shanmugavelandy, Sriram S, Fox, Todd, Mazza, Giuseppe, Argemi, Josepmaria, Bataller, Ramon, Cowart, Lauren Ashley, Kester, Mark, Pinzani, Massimo, and Rombouts, Krista

Abstract

In non-alcoholic steatohepatitis (NASH), many lines of investigation have reported a dysregulation in lipid homeostasis, leading to intrahepatic lipid accumulation. Recently, the role of dysfunctional sphingolipid metabolism has also been proposed. Human and animal models of NASH have been associated with elevated levels of long chain ceramides and pro-apoptotic sphingolipid metabolites, implicated in regulating fatty acid oxidation and inflammation. Importantly, inhibition of de novo ceramide biosynthesis or knock-down of ceramide synthases reverse some of the pathology of NASH. In contrast, cell permeable, short chain ceramides have shown anti-inflammatory actions in multiple models of inflammatory disease. Here, we investigated non-apoptotic doses of a liposome containing short chain C6-Ceramide (Lip-C6) administered to human hepatic stellate cells (hHSC), a key effector of hepatic fibrogenesis, and an animal model characterized by inflammation and elevated liver fat content. On the basis of the results from unbiased liver transcriptomic studies from non-alcoholic fatty liver disease patients, we chose to focus on adenosine monophosphate activated kinase (AMPK) and nuclear factor-erythroid 2-related factor (Nrf2) signaling pathways, which showed an abnormal profile. Lip-C6 administration inhibited hHSC proliferation while improving anti-oxidant protection and energy homeostasis, as indicated by upregulation of Nrf2, activation of AMPK and an increase in ATP. To confirm these in vitro data, we investigated the effect of a single tail-vein injection of Lip-C6 in the methionine-choline deficient (MCD) diet mouse model. Lip-C6, but not control liposomes, upregulated phospho-AMPK, without inducing liver toxicity, apoptosis, or exacerbating inflammatory signaling pathways. Alluding to mechanism, mass spectrometry lipidomics showed that Lip-C6-treatment reversed the imbalance in hepatic phosphatidylcholines and diacylglycerides species induced by the MCD-fed diet. These

Published
2020

22. Perturbations in Mitochondrial Dynamics Are Closely Involved in the Progression of Alcoholic Liver Disease

Author

Palma, Elena, Riva, Antonio, Moreno, Christophe, Odena, Gemma, Mudan, Satvinder, Manyakin, Nikolai, Miquel, Rosa, Degré, Delphine, Trepo, Eric, Sancho-Bru, Pau, Altamirano, Jose, Caballeria, Juan, Zamalloa, Ane, Menon, David Krishna, Heaton, Nigel, Williams, Roger, Bataller, Ramon, Chokshi, Shilpa, Palma, Elena, Riva, Antonio, Moreno, Christophe, Odena, Gemma, Mudan, Satvinder, Manyakin, Nikolai, Miquel, Rosa, Degré, Delphine, Trepo, Eric, Sancho-Bru, Pau, Altamirano, Jose, Caballeria, Juan, Zamalloa, Ane, Menon, David Krishna, Heaton, Nigel, Williams, Roger, Bataller, Ramon, and Chokshi, Shilpa

Abstract

Background: Mitochondria play a fundamental role in the pathogenesis of alcoholic liver disease (ALD). The preservation of functional mitochondria during toxic alcohol insults is essential for cell survival and is maintained by key processes known as mitochondrial dynamics, including fragmentation and fusion, which are regulated by mitochondria-shaping proteins (MSP). We have shown mitochondrial dynamics to be distorted by alcohol in cellular and animal models, but the effect in humans remains unknown. Methods: Hepatic gene expression of the main MSP involved in the mitochondrial fusion and fragmentation pathways was evaluated in patients with alcoholic hepatitis (AH) by DNA microarray (n = 15) and Reverse Transcription Polymerase Chain Reaction (n = 32). The activation of dynamin-1-like protein (Drp1) was also investigated in mitochondria isolated from liver biopsies of ALD patients (n = 8). The effects of alcohol on mitochondrial dynamics and on MSP protein expression were studied in human precision-cut liver slices (PCLS) exposed for 24 hours to increasing doses of ethanol (EtOH; 50 to 250 mM). Results: A profound hyperactivation of the fragmentation pathway was observed in AH patients, with a significant increase in the expression of Drp1 and its adapters/receptors. The translocation of Drp1 to the mitochondria was also induced in patients with severe ALD and was affected in the PCLS with short-term exposure to EtOH but only mildly. The fusion pathway was not altered in ALD, and this was confirmed in the PCLS model. Conclusions: The present study reveals the role of mitochondrial dynamics in human ALD, confirming our previous observations in animal and cell culture models of ALD. Taken together, we show that alcohol has a significant impact on the fragmentation pathway, and we confirm Drp1 as a potential therapeutic target in severe ALD., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2020

28. Exogenous Liposomal Ceramide-C6 Ameliorates Lipidomic Profile, Energy Homeostasis, and Anti-Oxidant Systems in NASH

Author

Zanieri, Francesca, primary, Levi, Ana, additional, Montefusco, David, additional, Longato, Lisa, additional, De Chiara, Francesco, additional, Frenguelli, Luca, additional, Omenetti, Sara, additional, Andreola, Fausto, additional, Luong, Tu Vinh, additional, Massey, Veronica, additional, Caballeria, Juan, additional, Fondevila, Constantino, additional, Shanmugavelandy, Sriram S, additional, Fox, Todd, additional, Mazza, Giuseppe, additional, Argemi, Josepmaria, additional, Bataller, Ramon, additional, Cowart, Lauren Ashley, additional, Kester, Mark, additional, Pinzani, Massimo, additional, and Rombouts, Krista, additional

Published
2020
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29. Perturbations in Mitochondrial Dynamics Are Closely Involved in the Progression of Alcoholic Liver Disease

Author

Palma, Elena, primary, Riva, Antonio, additional, Moreno, Christophe, additional, Odena, Gemma, additional, Mudan, Satvinder, additional, Manyakin, Nikolai, additional, Miquel, Rosa, additional, Degré, Delphine, additional, Trepo, Eric, additional, Sancho‐Bru, Pau, additional, Altamirano, Jose, additional, Caballeria, Juan, additional, Zamalloa, Ane, additional, Menon, Krishna, additional, Heaton, Nigel, additional, Williams, Roger, additional, Bataller, Ramon, additional, and Chokshi, Shilpa, additional

Published
2020
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33. A randomized, placebo-controlled trial of cenicriviroc for treatment of nonalcoholic steatohepatitis with fibrosis

Author

Friedman, Scott L., Ratziu, Vlad, Harrison, Stephen A., Abdelmalek, Manal F., Aithal, Guruprasad P., Caballeria, Juan, Francque, Sven, Farrell, Geoffrey, Kowdley, Kris V., Craxi, Antonio, Simon, Krzysztof, Fischer, Laurent, Melchor-Khan, Liza, Vest, Jeffrey, Wiens, Brian L., Vig, Pamela, Seyedkazemi, Star, Goodman, Zachary, Wong, Vincent Wai-Sun, Loomba, Rohit, Tacke, Frank, Sanyal, Arun, Lefebvre, Eric, Friedman, Scott L., Ratziu, Vlad, Harrison, Stephen A., Abdelmalek, Manal F., Aithal, Guruprasad P., Caballeria, Juan, Francque, Sven, Farrell, Geoffrey, Kowdley, Kris V., Craxi, Antonio, Simon, Krzysztof, Fischer, Laurent, Melchor-Khan, Liza, Vest, Jeffrey, Wiens, Brian L., Vig, Pamela, Seyedkazemi, Star, Goodman, Zachary, Wong, Vincent Wai-Sun, Loomba, Rohit, Tacke, Frank, Sanyal, Arun, and Lefebvre, Eric

Abstract

The aim of this study was to evaluate cenicriviroc (CVC), a dual antagonist of C-C chemokine receptor types 2 and 5, for treatment of nonalcoholic steatohepatitis (NASH) with liver fibrosis (LF). A randomized, double-blind, multinational phase 2b study enrolled subjects with NASH, a nonalcoholic fatty liver disease activity score (NAS) ≥4, and LF (stages 1-3, NASH Clinical Research Network) at 81 clinical sites. Subjects (N = 289) were randomly assigned CVC 150 mg or placebo. Primary outcome was ≥2-point improvement in NAS and no worsening of fibrosis at year 1. Key secondary outcomes were: resolution of steatohepatitis (SH) and no worsening of fibrosis; improvement in fibrosis by ≥1 stage and no worsening of SH. Biomarkers of inflammation and adverse events were assessed. Full study recruitment was achieved. The primary endpoint of NAS improvement in the intent-to-treat population and resolution of SH was achieved in a similar proportion of subjects on CVC (N = 145) and placebo (N = 144; 16% vs. 19%, P = 0.52 and 8% vs. 6%, P = 0.49, respectively). However, the fibrosis endpoint was met in significantly more subjects on CVC than placebo (20% vs. 10%; P = 0.02). Treatment benefits were greater in those with higher disease activity and fibrosis stage at baseline. Biomarkers of systemic inflammation were reduced with CVC. Safety and tolerability of CVC were comparable to placebo. Conclusion: After 1 year of CVC treatment, twice as many subjects achieved improvement in fibrosis and no worsening of SH compared with placebo. Given the urgent need to develop antifibrotic therapies in NASH, these findings warrant phase 3 evaluation.

Published
2018

41. Deregulated neddylation in liver fibrosis.

Author

Zubiete-Franco, Imanol, Zubiete-Franco, Imanol, Fernández-Tussy, Pablo, Barbier-Torres, Lucía, Simon, Jorge, Fernández-Ramos, David, Lopitz-Otsoa, Fernando, Gutiérrez-de Juan, Virginia, de Davalillo, Sergio López, Duce, Antonio Martín, Iruzubieta, Paula, Taibo, Daniel, Crespo, Javier, Caballeria, Juan, Villa, Erica, Aurrekoetxea, Igor, Aspichueta, Patricia, Varela-Rey, Marta, Lu, Shelly C, Mato, José M, Beraza, Naiara, Delgado, Teresa C, Martínez-Chantar, María L, Zubiete-Franco, Imanol, Zubiete-Franco, Imanol, Fernández-Tussy, Pablo, Barbier-Torres, Lucía, Simon, Jorge, Fernández-Ramos, David, Lopitz-Otsoa, Fernando, Gutiérrez-de Juan, Virginia, de Davalillo, Sergio López, Duce, Antonio Martín, Iruzubieta, Paula, Taibo, Daniel, Crespo, Javier, Caballeria, Juan, Villa, Erica, Aurrekoetxea, Igor, Aspichueta, Patricia, Varela-Rey, Marta, Lu, Shelly C, Mato, José M, Beraza, Naiara, Delgado, Teresa C, and Martínez-Chantar, María L

Abstract

Hepatic fibrosis is a global health problem currently without effective therapeutic approaches. Even though the ubiquitin-like posttranslational modification of neddylation, that conjugates Nedd8 (neural precursor cell expressed developmentally downregulated) to specific targets, is aberrant in many pathologies, its relevance in liver fibrosis (LF) remained unexplored. Our results show deregulated neddylation in clinical fibrosis and both in mouse bileductligation- and CCl4 -induced fibrosis. Importantly, neddylation inhibition, by using the pharmacological inhibitor, MLN4924, reduced liver injury, apoptosis, inflammation, and fibrosis by targeting different hepatic cell types. On one hand, increased neddylation was associated with augmented caspase 3 activity in bile-acid-induced apoptosis in mouse hepatocytes whereas neddylation inhibition ameliorated apoptosis through reduction of expression of the Cxcl1 and Ccl2 chemokines. On the other hand, chemokine receptors and cytokines, usually induced in activated macrophages, were reduced after neddylation inhibition in mouse Kupffer cells. Under these circumstances, decreased hepatocyte cell death and inflammation after neddylation inhibition could partly account for reduction of hepatic stellate cell (HSC) activation. We provide evidence that augmented neddylation characterizes activated HSCs, suggesting that neddylation inhibition could be important for resolving LF by directly targeting these fibrogenic cells. Indeed, neddylation inhibition in activated HSCs induces apoptosis in a process partly mediated by accumulation of c-Jun, whose cullin-mediated degradation is impaired under these circumstances.ConclusionNeddylation inhibition reduces fibrosis, suggesting neddylation as a potential and attractive therapeutic target in liver fibrosis. (Hepatology 2017;65:694-709).

Published
2017

45. Corrigendum: A Day-4 Lille Model Predicts Response to Corticosteroids and Mortality in Severe Alcoholic Hepatitis

Author

Garcia-Saenz-de-Sicilia, Mauricio, primary, Duvoor, Chitharanjan, additional, Altamirano, Jose, additional, Chavez-Araujo, Roberta, additional, Prado, Veronica, additional, de Lourdes Candolo-Martinelli, Ana, additional, Holanda-Almeida, Patricia, additional, Becerra-Martins-de-Oliveira, Bernardo, additional, Fernandez-de-Almeida, Simony, additional, Bataller, Ramón, additional, Caballeria, Juan, additional, and Duarte-Rojo, Andres, additional

Published
2017
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46. A Day-4 Lille Model Predicts Response to Corticosteroids and Mortality in Severe Alcoholic Hepatitis

Author

Garcia-Saenz-de-Sicilia, Mauricio, primary, Duvoor, Chitharanjan, additional, Altamirano, Jose, additional, Chavez-Araujo, Roberta, additional, Prado, Veronica, additional, de Lourdes Candolo-Martinelli, Ana, additional, Holanda-Almeida, Patricia, additional, Becerra-Martins-de-Oliveira, Bernardo, additional, Fernandez-de-Almeida, Simony, additional, Bataller, Ramón, additional, Caballeria, Juan, additional, and Duarte-Rojo, Andres, additional

Published
2017
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47. Deregulated neddylation in liver fibrosis

Author

Zubiete‐Franco, Imanol, primary, Fernández‐Tussy, Pablo, additional, Barbier‐Torres, Lucía, additional, Simon, Jorge, additional, Fernández‐Ramos, David, additional, Lopitz‐Otsoa, Fernando, additional, Gutiérrez‐de Juan, Virginia, additional, de Davalillo, Sergio López, additional, Duce, Antonio Martín, additional, Iruzubieta, Paula, additional, Taibo, Daniel, additional, Crespo, Javier, additional, Caballeria, Juan, additional, Villa, Erica, additional, Aurrekoetxea, Igor, additional, Aspichueta, Patricia, additional, Varela‐Rey, Marta, additional, Lu, Shelly C, additional, Mato, José M., additional, Beraza, Naiara, additional, Delgado, Teresa C., additional, and Martínez‐Chantar, María L, additional

Published
2016
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48. 246 – Intestinal Fungal Dysbiosis and Systemic Immune Response to Fungi in Patients with Alcoholic Hepatitis

Author

Lang, Sonja, Duan, Yi, Liu, Jinyuan, Ventura-Cots, Meritxell, Lucey, Michael R., Padilla, Francisco J. Bosques, Mathurin, Philippe, Louvet, Alexandre, Garcia-Tsao, Guadalupe, Verna, Elizabeth C., Abraldes, Juan, Brown, Robert S., Vargas, Victor, Altamirano, Jose, Caballería, Juan, Shawcross, Debbie, Ho, Samuel B., Bataller, Ramon, Tu, Xin, Stärkel, Peter, Fouts, Derrick E., and Schnabl, Bernd

Published
2019
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49. PS-200-The combination of HEPAmet fibrosis score and transient elastography shows a high diagnostic accuracy in predicting advanced fibrosis in NAFLD

Author

Ampuero, Javier, Aller, Rocío, Gallego-Durán, Rocío, Calleja Panero, José Luis, Boursier, Jerome, Petta, Salvatore, Benlloch, Salvador, Crespo, Javier, Ming-Hua, Zheng, Gómez-Camarero, Judith, Augustin, Salvador, Escudero-García, Desamparados, Albillos, Agustin, Diago, Moises, Iacono, Oreste Lo, Caballería, Juan, Turnés, Juan, Francés, Rubén, and Gomez, Manuel Romero

Published
2019
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