AI Article Synopsis

  • HDAC3 and NCoR1/2 are crucial epigenetic regulators that influence gene expression and metabolism by acting as transcriptional co-repressors.
  • Genetic deletion of HDAC3 and NCoR1 in mice has shown improved glucose tolerance and insulin sensitivity, indicating their significant roles in managing metabolic processes.
  • Disruption of the HDAC3/NCoR1/2 complex is linked to cardio-metabolic diseases like obesity and type 2 diabetes, highlighting the potential for targeting this pathway in future therapies.

Article Abstract

Histone deacetylase 3 (HDAC3) and nuclear receptor co-repressor (NCoR1/2) are epigenetic regulators that play a key role in gene expression and metabolism. HDAC3 is a class I histone deacetylase that functions as a transcriptional co-repressor, modulating gene expression by removing acetyl groups from histones and non-histone proteins. NCoR1, on the other hand, is a transcriptional co-repressor that interacts with nuclear hormone receptors, including peroxisome proliferator-activated receptor gamma (PPARγ) and liver X receptor (LXR), to regulate metabolic gene expression. Recent research has revealed a functional link between HDAC3 and NCoR1 in the regulation of metabolic gene expression. Genetic deletion of HDAC3 in mouse models has been shown to improve glucose intolerance and insulin sensitivity in the liver, skeletal muscle, and adipose tissue. Similarly, genetic deletion of NCoR1 has improved insulin resistance and reduced adiposity in mouse models. Dysregulation of this interaction has been associated with the development of cardio-metabolic diseases such as cardiovascular diseases, obesity and type 2 diabetes, suggesting that targeting this pathway may hold promise for the development of novel therapeutic interventions. In this review, we summarize the current understanding of individual functions of HDAC3 and NCoR1/2 and the co-repressor complex formation (HDAC3/NCoR1/2) in different metabolic tissues. Further studies are needed to thoroughly understand the mechanisms through which HDAC3, and NCoR1/2 govern metabolic processes and the implications for treating metabolic diseases.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10477789PMC
http://dx.doi.org/10.3389/fmolb.2023.1190094DOI Listing

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