4.6 Review

Immune-related pathogenesis and therapeutic strategies of nonalcoholic steatohepatitis

Journal

ARCHIVES OF PHARMACAL RESEARCH
Volume 45, Issue 4, Pages 229-244

Publisher

PHARMACEUTICAL SOC KOREA
DOI: 10.1007/s12272-022-01379-1

Keywords

Fatty liver; Nonalcoholic steatohepatitis; Immune cells; Chemokines; Inflammation

Funding

  1. National Research Foundation of Korea (NRF) - Korea Government (MSIT) [2021R1F1A1056033, 2022R1C1C1003563]
  2. National Research Foundation of Korea [2022R1C1C1003563, 2021R1F1A1056033] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome and is prevalent worldwide due to the obesity pandemic. NAFLD includes fatty liver, nonalcoholic steatohepatitis (NASH), cirrhosis, and carcinoma. Excessive fat accumulation induces fatty liver, while the progression to NASH involves various complex factors. Inflammation and fibrosis, closely associated with immune cells and immunological factors, differentiate fatty liver from NASH. Thus, understanding the immunological mechanisms contributing to NASH pathogenesis is crucial for the identification of therapeutic targets and the development of viable treatments.
Nonalcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome and has become prevalent in the adult population worldwide, given the ongoing obesity pandemic. NAFLD comprises several hepatic disorders, ranging from fatty liver to nonalcoholic steatohepatitis (NASH), cirrhosis, and carcinoma. Excessive fat accumulation in the liver can induce the development of fatty liver, whereas the progression of fatty liver to NASH involves various complex factors. The crucial difference between fatty liver and NASH is the presence of inflammation and fibrosis, the emergence of which is closely associated with the action of immune cells and immunological factors, such as chemokines and cytokines. Thus, expanding our understanding of immunological mechanisms contributing to NASH pathogenesis will lead to the identification of therapeutic targets and the development of viable therapeutics against NASH.

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