Review Article Open Access
Volume 2 | Issue 3 | DOI: https://doi.org/10.33696/Signaling.2.049

Function of Mitogen-Activated Protein Kinases in Hepatic Inflammation

  • 1Department of Biological Sciences, University of Alabama in Huntsville, Huntsville, Alabama 35899, USA
  • 2Division of Kinesiology, University of Texas at El Paso, El Paso, Texas 79968, USA
  • 3Department of Aging and Geriatric Research, Institute of Aging, College of Medicine, University of Florida, Gainesville, Florida 32610, USA
+ Affiliations - Affiliations

Corresponding Author

Ahmed Lawan, al0122@uah.edu

Received Date: July 08, 2021

Accepted Date: August 23, 2021


The western diet and overuse of anti-inflammatory medication have caused a great deal of stress on the liver. Obesity and the associated inflammatory state in insulin-responsive tissues result in the release of pro-inflammatory cytokine that activates the stress-responsive MAPKs, p38 MAPK, and JNK. These MAPKs have figured prominently as critical effectors in physiological and pathophysiological hepatic inflammation. In contrast, evidence for a role for ERK1/2 in hepatic inflammation has been less well developed. In this review article, we describe recent insights into the physiology and pathophysiology of the role of stress-responsive MAPKs in hepatic inflammation during obesity and liver injury with a focus on macrophages, hepatocytes and hepatic stellate cells. In response to metabolic stress and liver injury, JNK activation in macrophages and hepatocytes promotes the secretion of inflammatory cytokines and macrophage and neutrophil infiltration. p38 MAPK plays an important role in contributing to the progression of hepatic inflammation in response to various hepatic cellular stresses, although the precise substrates mediating these effects in hepatocytes and hepatic stellate cells remain to be identified. Both JNK and p38 MAPK promotes profibrotic behavior in hepatic stellate cells.


MAP kinase, Hepatic inflammation, Obesity, Liver injury

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