Erratum to: “MLKL-dependent signaling regulates autophagic flux in a murine model of non-alcoholic-associated fatty liver and steatohepatitis (J Hepatol 2020; 73: 616–627)”

Xiaoqin Wu; Kyle L. Poulsen; Carlos Sanz-Garcia; Emily Huang; Megan R. McMullen; Sanjoy Roychowdhury; Srinivasan Dasarathy; Laura E. Nagy

doi:10.1016/j.jhep.2021.01.006

Erratum to: “MLKL-dependent signaling regulates autophagic flux in a murine model of non-alcoholic-associated fatty liver and steatohepatitis (J Hepatol 2020; 73: 616–627)”

Xiaoqin Wu
Xiaoqin Wu
Affiliations
Center for Liver Disease Research, Department of Inflammation and Immunity, Cleveland Clinic, Cleveland, OH, United States
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Kyle L. Poulsen
Kyle L. Poulsen
Affiliations
Center for Liver Disease Research, Department of Inflammation and Immunity, Cleveland Clinic, Cleveland, OH, United States
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Carlos Sanz-Garcia
Carlos Sanz-Garcia
Affiliations
Center for Liver Disease Research, Department of Inflammation and Immunity, Cleveland Clinic, Cleveland, OH, United States
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Emily Huang
Emily Huang
Affiliations
Center for Liver Disease Research, Department of Inflammation and Immunity, Cleveland Clinic, Cleveland, OH, United States
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Megan R. McMullen
Megan R. McMullen
Affiliations
Center for Liver Disease Research, Department of Inflammation and Immunity, Cleveland Clinic, Cleveland, OH, United States
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Sanjoy Roychowdhury
Sanjoy Roychowdhury
Affiliations
Center for Liver Disease Research, Department of Inflammation and Immunity, Cleveland Clinic, Cleveland, OH, United States
Department of Molecular Medicine, Case Western Reserve University, Cleveland, OH, United States
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Srinivasan Dasarathy
Srinivasan Dasarathy
Affiliations
Center for Liver Disease Research, Department of Inflammation and Immunity, Cleveland Clinic, Cleveland, OH, United States
Department of Gastroenterology and Hepatology, Cleveland Clinic, Cleveland, OH, United States
Department of Molecular Medicine, Case Western Reserve University, Cleveland, OH, United States
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Laura E. Nagy
Laura E. Nagy
Correspondence
Corresponding author. Address: Cleveland Clinic, Lerner Research Institute/NE40, 9500 Euclid Ave, Cleveland OH 44195, USA. Tel.: 216-444-4021, fax: 216-636-1493.
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Affiliations
Center for Liver Disease Research, Department of Inflammation and Immunity, Cleveland Clinic, Cleveland, OH, United States
Department of Gastroenterology and Hepatology, Cleveland Clinic, Cleveland, OH, United States
Department of Molecular Medicine, Case Western Reserve University, Cleveland, OH, United States
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Published:January 29, 2021DOI:https://doi.org/10.1016/j.jhep.2021.01.006

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MLKL-dependent signaling regulates autophagic flux in a murine model of non-alcohol-associated fatty liver and steatohepatitis
Journal of HepatologyVol. 73Issue 3
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  Autophagy maintains cellular homeostasis and plays a critical role in the development of non-alcoholic fatty liver and steatohepatitis. The pseudokinase mixed lineage kinase domain-like (MLKL) is a key downstream effector of receptor interacting protein kinase 3 (RIP3) in the necroptotic pathway of programmed cell death. However, recent data reveal that MLKL also regulates autophagy. Herein, we tested the hypothesis that MLKL contributes to the progression of Western diet-induced liver injury in mice by regulating autophagy.
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It has come to our attention that there was a mistake in Fig. 7 in the published version of our manuscript. The mistake occurred during the publication process and has resulted to a duplicated ‘Mlkl plasmid’ image within the panel in Fig. 7B. Please see the corrected figure below. We apologize for any inconvenience caused.

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Published online: January 29, 2021

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DOI: https://doi.org/10.1016/j.jhep.2021.01.006

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Erratum to: “MLKL-dependent signaling regulates autophagic flux in a murine model of non-alcoholic-associated fatty liver and steatohepatitis (J Hepatol 2020; 73: 616–627)”

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