Apoptosis and non-alcoholic fatty liver diseases

Tatsuo Kanda, Shunichi Matsuoka, Motomi Yamazaki, Toshikatsu Shibata, Kazushige Nirei, Hiroshi Takahashi, Tomohiro Kaneko, Mariko Fujisawa, Teruhisa Higuchi, Hitomi Nakamura, Naoki Matsumoto, Hiroaki Yamagami, Masahiro Ogawa, Hiroo Imazu, Kazumichi Kuroda, Mitsuhiko Moriyama

Research output: Contribution to journalReview articlepeer-review

204 Citations (Scopus)


The number of patients with nonalcoholic fatty liver diseases (NAFLD) including nonalcoholic steatohepatitis (NASH), has been increasing. NASH causes cirrhosis and hepatocellular carcinoma (HCC) and is one of the most serious health problems in the world. The mechanism through which NASH progresses is still largely unknown. Activation of caspases, Bcl-2 family proteins, and c-Jun N-terminal kinase-induced hepatocyte apoptosis plays a role in the activation of NAFLD/NASH. Apoptotic hepatocytes stimulate immune cells and hepatic stellate cells toward the progression of fibrosis in the liver through the production of inflammasomes and cytokines. Abnormalities in glucose and lipid metabolism as well as microbiota accelerate these processes. The production of reactive oxygen species, oxidative stress, and endoplasmic reticulum stress is also involved. Cell death, including apoptosis, seems very important in the progression of NAFLD and NASH. Recently, inhibitors of apoptosis have been developed as drugs for the treatment of NASH and may prevent cirrhosis and HCC. Increased hepatocyte apoptosis may distinguish NASH from NAFLD, and the improvement of apoptosis could play a role in controlling the development of NASH. In this review, the association between apoptosis and NAFLD/NASH are discussed. This review could provide their knowledge, which plays a role in seeing the patients with NAFLD/NASH in daily clinical practice.

Original languageEnglish
Pages (from-to)2661-2672
Number of pages12
JournalWorld Journal of Gastroenterology
Issue number25
Publication statusPublished - 7 Jul 2018


  • Apoptosis
  • Autophagy
  • C-Jun N-terminal kinase
  • Nonalcoholic fatty liver diseases
  • Nonalcoholic steatohepatitis


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