The pivotal role of heme Oxygenase-1 in reversing the pathophysiology and systemic complications of NAFLD. Review uri icon

Overview

abstract

  • The pathogenesis and molecular pathways involved in non-alcoholic fatty liver disease (NAFLD) are reviewed, as well as what is known about mitochondrial dysfunction that leads to heart disease and the progression to steatohepatitis and hepatic fibrosis. We focused our discussion on the role of the antioxidant gene heme oxygenase-1 (HO-1) and its nuclear coactivator, peroxisome proliferator-activated receptor-gamma coactivator (PGC1-α) in the regulation of mitochondrial biogenesis and function and potential therapeutic benefit for cardiac disease, NAFLD as well as the pharmacological effect they have on the chronic inflammatory state of obesity. The result is increased mitochondrial function and the conversion of white adipocyte tissue to beige adipose tissue ("browning of white adipose tissue") that leads to an improvement in signaling pathways and overall liver function. Improved mitochondrial biogenesis and function is essential to preventing the progression of hepatic steatosis to NASH and cirrhosis as well as preventing cardiovascular complications.

publication date

  • November 26, 2020

Research

keywords

  • Heme Oxygenase-1
  • Non-alcoholic Fatty Liver Disease

Identity

Scopus Document Identifier

  • 85097072017

Digital Object Identifier (DOI)

  • 10.1016/j.abb.2020.108679

PubMed ID

  • 33248947

Additional Document Info

volume

  • 697