Perspectives on cellular dysfunction in nonalcoholic steatohepatitis: a case of ‘multiorganelle failure’? Proceedings of a virtual workshop on nonalcoholic steatohepatitis

Figures & data

Figure 1. A model of the pathogenesis of nonalcoholic steatohepatitis.

Insulin resistance occurs as an early inciting event in the pathogenesis of NASH. It is fully acceptable that, once triggered, the pathogenic cascade of events will proceed independent of the initial offending agent, insulin resistance, accounting for the finding that agents aimed at combating it will not necessarily result in the interruption of ongoing liver damage. This results in NASH from ‘multiorganelle failure’, as described in the proceedings of this special focus issue.

FFA: Free fatty acid; NAFLD: Nonalcoholic fatty liver disease; NASH: Nonalcoholic steatohepatitis; ROS: Reactive oxygen species.

Reprinted from [30].

Arrese M. Burning hepatic fat: therapeutic potential for liver-specific thyromimetics in the treatment of nonalcoholic fatty liver disease. Hepatology49, 348–351 (2009).

 PubMed Web of Science ®Google Scholar