Literature DB >> 26870930

Targeting Cell Death and Sterile Inflammation Loop for the Treatment of Nonalcoholic Steatohepatitis.

Alexander Wree1, Wajahat Z Mehal2, Ariel E Feldstein1.   

Abstract

Nonalcoholic fatty liver disease represents a wide spectrum of conditions and is currently the most common form of chronic liver disease affecting both adults and children in the United States and many other parts of the world. Great effort has been focused on the development of novel therapies for those patients with the more advanced forms of the disease, in particular those with nonalcoholic steatohepatitis (NASH) and liver fibrosis that can be associated with significant morbidity and mortality. In this review, the authors focus on the role of cell death and sterile inflammatory pathways as well as the self-perpetuating deleterious cycle they may trigger as novel therapeutic targets for the treatment of fibrotic NASH. Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

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Year:  2016        PMID: 26870930      PMCID: PMC4955833          DOI: 10.1055/s-0035-1571272

Source DB:  PubMed          Journal:  Semin Liver Dis        ISSN: 0272-8087            Impact factor:   6.115


  99 in total

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7.  First clinical trial of a novel caspase inhibitor: anti-apoptotic caspase inhibitor, IDN-6556, improves liver enzymes.

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8.  Essential role of matrix metalloproteinases in interleukin-1-induced myofibroblastic activation of hepatic stellate cell in collagen.

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9.  MLK3 as a regulator of disease progression in Non-alcoholic steatohepatitis.

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10.  Divergent effects of RIP1 or RIP3 blockade in murine models of acute liver injury.

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Journal:  Cell Death Dis       Date:  2015-05-07       Impact factor: 8.469

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  11 in total

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Review 2.  Non-alcoholic fatty liver disease.

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7.  Efficacy and Safety of Emricasan in Liver Cirrhosis and/or Fibrosis.

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Review 8.  Liver Fibrosis: Mechanistic Concepts and Therapeutic Perspectives.

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Review 9.  The Role of NLRP3 Inflammasome in Radiation-Induced Cardiovascular Injury.

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10.  Hepatic neuregulin 4 signaling defines an endocrine checkpoint for steatosis-to-NASH progression.

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