Role of TRAF3 in neurological and cardiovascular diseases: an overview of recent studies

Biomol Concepts. 2017 Sep 26;8(3-4):197-202. doi: 10.1515/bmc-2017-0008.

Abstract

Tumour necrosis factor receptor-associated factor 3 (TRAF3) is a member of the TRAF adaptor protein family, which exerts different effects on the cell depending on the receptor to which it binds and the cell type in which it is expressed. TRAF3 is a major regulator of the innate immune response. To perform its functions properly, TRAF3 is transcriptionally and epigenetically regulated. At the transcriptional level, TRAF3 expression has been associated with neurological and cardiovascular diseases including stroke, among other pathologies. Epigenetic modifications of TRAF3 have been observed at the histone and DNA levels. It has been observed that acetylation of TRAF3, as well as other NF-κβ target genes, is associated with cardiac hypertrophy. Furthermore, TRAF3 methylation has been associated with vascular recurrence after ischemic stroke in patients treated with clopidogrel. In this overview, we summarise the most interesting studies related to transcriptional and epigenetic regulation of TRAF3 focusing on those studies performed in neurological and cardiovascular diseases.

Keywords: EWAS; TRAF3; epigenetics; genetics; stroke.

MeSH terms

  • Acetylation
  • Cardiovascular Diseases / metabolism*
  • Epigenesis, Genetic
  • Humans
  • Methylation
  • NF-kappa B / metabolism
  • Nervous System Diseases / metabolism*
  • Signal Transduction
  • TNF Receptor-Associated Factor 3 / metabolism
  • TNF Receptor-Associated Factor 3 / physiology*
  • Transcription Factor AP-1 / metabolism

Substances

  • NF-kappa B
  • TNF Receptor-Associated Factor 3
  • TRAF3 protein, human
  • Transcription Factor AP-1