Nonalcoholic Steatohepatitis Promoting Kinases

Research output: Contribution to journalArticlepeer-review

Abstract

Nonalcoholic hepatitis (NASH) is the progressive inflammatory form of nonalcoholic fatty liver disease. Although the mechanisms of hepatic inflammation in NASH remain incompletely understood, emerging literature implicates the proinflammatory environment created by toxic lipid-induced hepatocyte injury, termed lipotoxicity. Interestingly, numerous NASH-promoting kinases in hepatocytes, immune cells, and adipocytes are activated by the lipotoxic insult associated with obesity. In the current review, we discuss recent advances in NASH-promoting kinases as disease mediators and therapeutic targets. The focus of the review is mainly on the mitogen-activated protein kinases including mixed lineage kinase 3, apoptosis signal-regulating kinase 1, c-Jun N-terminal kinase, and p38 MAPK; the endoplasmic reticulum (ER) stress kinases protein kinase RNA-like ER kinase and inositol-requiring protein-1α; as well as the Rho-associated protein kinase 1. We also discuss various pharmacological agents targeting these stress kinases in NASH that are under different phases of development.

Original languageEnglish (US)
Pages (from-to)346-357
Number of pages12
JournalSeminars in liver disease
Volume40
Issue number4
DOIs
StatePublished - Nov 1 2020

Keywords

  • Rho-associated protein kinase
  • endoplasmic reticulum stress
  • mitogen-activated protein kinases
  • nonalcoholic steatohepatitis

ASJC Scopus subject areas

  • Hepatology

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