Oxidative stress in nonalcoholic steatohepatitis

Akinobu Takaki, Daisuke Uchida, Kazuhide Yamamoto

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Nonalcoholic fatty liver disease (NAFLD) is a disease with increasing prevalence that is potentially lethal after decades of persistent fat toxicity on the liver and accompanying organs. The pathogenesis for the progression of benign nonalcoholic fatty liver (NAFL) to progressive nonalcoholic steatohepatitis (NASH) is acknowledged as a multiple parallel hit process, including fat deposition, genetic factors, insulin resistance, and oxidative stress. Oxidative stress is one of the main pathogenic factors driving the progression of NAFL to NASH. Excessive accumulation of long chain fatty acids results in activation of the mitochondrial b-oxidation pathway and consequent reactive oxygen species (ROS) production. ROS can mediate oxidative stress responses in hepatocytes, Kupffer cells and hepatic stellate cells (HSCs), resulting in hepatocyte damage as well as proinflammatory and profibrogenic responses. ROS detoxification pathway signaling is often damaged in NAFLD following ROS accumulation. Inactivation of the prooxidant production pathway is presently the primary treatment strategy. However, as oxidative stress is an essential response in living organisms, a new treatment strategy that activates toxic oxidative stress detoxifying pathways while maintaining essential oxidative stress responses is preferred.

Original languageEnglish
Title of host publicationReactive Oxygen Species in Biology and Human Health
PublisherCRC Press
Pages349-361
Number of pages13
ISBN (Electronic)9781498735469
ISBN (Print)9781498735452
DOIs
Publication statusPublished - Jan 1 2017

Fingerprint

Oxidative stress
Oxidative Stress
Liver
Reactive Oxygen Species
Hepatocytes
Fats
Hepatic Stellate Cells
Detoxification
Kupffer Cells
Poisons
Toxicity
Insulin Resistance
Non-alcoholic Fatty Liver Disease
Fatty Acids
Chemical activation
Insulin
Oxidation

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

Takaki, A., Uchida, D., & Yamamoto, K. (2017). Oxidative stress in nonalcoholic steatohepatitis. In Reactive Oxygen Species in Biology and Human Health (pp. 349-361). CRC Press. https://doi.org/10.1201/b20228

Oxidative stress in nonalcoholic steatohepatitis. / Takaki, Akinobu; Uchida, Daisuke; Yamamoto, Kazuhide.

Reactive Oxygen Species in Biology and Human Health. CRC Press, 2017. p. 349-361.

Research output: Chapter in Book/Report/Conference proceedingChapter

Takaki, A, Uchida, D & Yamamoto, K 2017, Oxidative stress in nonalcoholic steatohepatitis. in Reactive Oxygen Species in Biology and Human Health. CRC Press, pp. 349-361. https://doi.org/10.1201/b20228
Takaki A, Uchida D, Yamamoto K. Oxidative stress in nonalcoholic steatohepatitis. In Reactive Oxygen Species in Biology and Human Health. CRC Press. 2017. p. 349-361 https://doi.org/10.1201/b20228
Takaki, Akinobu ; Uchida, Daisuke ; Yamamoto, Kazuhide. / Oxidative stress in nonalcoholic steatohepatitis. Reactive Oxygen Species in Biology and Human Health. CRC Press, 2017. pp. 349-361
@inbook{4a7a86f68d5242cfa3961b96e5dad22e,
title = "Oxidative stress in nonalcoholic steatohepatitis",
abstract = "Nonalcoholic fatty liver disease (NAFLD) is a disease with increasing prevalence that is potentially lethal after decades of persistent fat toxicity on the liver and accompanying organs. The pathogenesis for the progression of benign nonalcoholic fatty liver (NAFL) to progressive nonalcoholic steatohepatitis (NASH) is acknowledged as a multiple parallel hit process, including fat deposition, genetic factors, insulin resistance, and oxidative stress. Oxidative stress is one of the main pathogenic factors driving the progression of NAFL to NASH. Excessive accumulation of long chain fatty acids results in activation of the mitochondrial b-oxidation pathway and consequent reactive oxygen species (ROS) production. ROS can mediate oxidative stress responses in hepatocytes, Kupffer cells and hepatic stellate cells (HSCs), resulting in hepatocyte damage as well as proinflammatory and profibrogenic responses. ROS detoxification pathway signaling is often damaged in NAFLD following ROS accumulation. Inactivation of the prooxidant production pathway is presently the primary treatment strategy. However, as oxidative stress is an essential response in living organisms, a new treatment strategy that activates toxic oxidative stress detoxifying pathways while maintaining essential oxidative stress responses is preferred.",
author = "Akinobu Takaki and Daisuke Uchida and Kazuhide Yamamoto",
year = "2017",
month = "1",
day = "1",
doi = "10.1201/b20228",
language = "English",
isbn = "9781498735452",
pages = "349--361",
booktitle = "Reactive Oxygen Species in Biology and Human Health",
publisher = "CRC Press",

}

TY - CHAP

T1 - Oxidative stress in nonalcoholic steatohepatitis

AU - Takaki, Akinobu

AU - Uchida, Daisuke

AU - Yamamoto, Kazuhide

PY - 2017/1/1

Y1 - 2017/1/1

N2 - Nonalcoholic fatty liver disease (NAFLD) is a disease with increasing prevalence that is potentially lethal after decades of persistent fat toxicity on the liver and accompanying organs. The pathogenesis for the progression of benign nonalcoholic fatty liver (NAFL) to progressive nonalcoholic steatohepatitis (NASH) is acknowledged as a multiple parallel hit process, including fat deposition, genetic factors, insulin resistance, and oxidative stress. Oxidative stress is one of the main pathogenic factors driving the progression of NAFL to NASH. Excessive accumulation of long chain fatty acids results in activation of the mitochondrial b-oxidation pathway and consequent reactive oxygen species (ROS) production. ROS can mediate oxidative stress responses in hepatocytes, Kupffer cells and hepatic stellate cells (HSCs), resulting in hepatocyte damage as well as proinflammatory and profibrogenic responses. ROS detoxification pathway signaling is often damaged in NAFLD following ROS accumulation. Inactivation of the prooxidant production pathway is presently the primary treatment strategy. However, as oxidative stress is an essential response in living organisms, a new treatment strategy that activates toxic oxidative stress detoxifying pathways while maintaining essential oxidative stress responses is preferred.

AB - Nonalcoholic fatty liver disease (NAFLD) is a disease with increasing prevalence that is potentially lethal after decades of persistent fat toxicity on the liver and accompanying organs. The pathogenesis for the progression of benign nonalcoholic fatty liver (NAFL) to progressive nonalcoholic steatohepatitis (NASH) is acknowledged as a multiple parallel hit process, including fat deposition, genetic factors, insulin resistance, and oxidative stress. Oxidative stress is one of the main pathogenic factors driving the progression of NAFL to NASH. Excessive accumulation of long chain fatty acids results in activation of the mitochondrial b-oxidation pathway and consequent reactive oxygen species (ROS) production. ROS can mediate oxidative stress responses in hepatocytes, Kupffer cells and hepatic stellate cells (HSCs), resulting in hepatocyte damage as well as proinflammatory and profibrogenic responses. ROS detoxification pathway signaling is often damaged in NAFLD following ROS accumulation. Inactivation of the prooxidant production pathway is presently the primary treatment strategy. However, as oxidative stress is an essential response in living organisms, a new treatment strategy that activates toxic oxidative stress detoxifying pathways while maintaining essential oxidative stress responses is preferred.

UR - http://www.scopus.com/inward/record.url?scp=85051951202&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85051951202&partnerID=8YFLogxK

U2 - 10.1201/b20228

DO - 10.1201/b20228

M3 - Chapter

SN - 9781498735452

SP - 349

EP - 361

BT - Reactive Oxygen Species in Biology and Human Health

PB - CRC Press

ER -