PPARs in the Alcoholic Liver Disease

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (30 September 2020) | Viewed by 206

Special Issue Editor


E-Mail Website
Guest Editor
Cedars-Sinai Medical Center, Los Angeles, CA, USA
Interests: alcoholic liver disease; oxidative stress; hepatocellular carcinoma liver fibrosis; NASH; SUMOylation; phosphorylation; ubiquitination

Special Issue Information

Dear Colleagues,

The peroxisome proliferator-activated receptors (PPAR) are ligand-activated transcription factors that are known to have critical roles in the regulation of lipid homeostasis. Three PPAR isoforms, designated PPARα, -β/δ, and -γ have been identified.

The relationships between ethanol treatment and decreases of hepatic PPARα in mouse and human liver have been demonstrated. PPARα -null mice fed a diet containing a low concentration of ethanol exhibit marked symptoms similar to those observed in patients with alcoholic liver disease (ALD), including hepatomegaly, steatosis, elevated serum aspartate aminotiansferase and alanine aminotransferase levels, inflammation, spotty necrosis, centrilobular fibrosis and apoptosis.

PPARα seems to regulate the expression of the variety of proteins directly or indirectly liked to the increased susceptibility of human and mouse liver to alcohol-induced liver disease regulating the lipid metabolism, controlling the expression of genes involved in the transport, oxidation and export of free fatty acids. Since fatty liver represents a very common finding in ALD, the effect of ethanol metabolism on PPARα regulated processes has been intensively investigated in the past ten years.

Several studies demonstrated the importance of PPARγ in the activation of hepatic stellate cells (HSC). Active PPARγ is required for the maintenance of the resting “fat storing” phenotype by HSC, and its expression and transcriptional activity decrease during cell activation in culture.

PPAR-β/δ is probably the less characterized isoform of the PPAR family. Recent reports demonstrated the role for PPAR-β/δ in the regulation of glucose metabolism insulin sensitivity and the protective effects of PPAR-β/δ agonist on ethanol-induced liver injury.

Dysregulation of PPARs activity plays a central role in the onset and perpetuation of the mechanisms underlying all steps of the clinical progression in ALD.

In this special issue of Biomolecules called “PPARs in the Alcoholic Liver Disease” we would like to invite authors to submit original research articles as well as review articles that will help in understanding physiological and pathological roles of PPARs in ALD.

Dr. Tomasi Maria Lauda, Ph.D
Guest Editor

 

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Keywords

  • alcohol
  • PPARs
  • liver
  • ALD
  • steatosis
  • inflammation
  • hepatocellular carcinoma

Published Papers

There is no accepted submissions to this special issue at this moment.
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