4.7 Review

O-GlcNAcylation, enemy or ally during cardiac hypertrophy development?

Journal

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
Volume 1862, Issue 12, Pages 2232-2243

Publisher

ELSEVIER
DOI: 10.1016/j.bbadis.2016.08.012

Keywords

Cardiac hypertrophy; Protein O-GlcNAcylation; Cardiac disease; Diabetes; Glucose

Funding

  1. Fund for Scientific Research in Industry and Agriculture (FRIA), Belgium
  2. Fonds de Recherche Clinique from Universite catholique de Louvain (UCL), Belgium
  3. Fonds National de la Recherche Scientifique et Medicale, Belgium [T.0105.14]
  4. Action de Recherche Concertee, UCL, Belgium
  5. AstraZeneca, Belgium

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O-linked attachment of the monosaccharide beta-N-acetyl-glucosamine (O-GlcNAcylation) is a post-translational modification occurring on serine and threonine residues, which is evolving as an important mechanism for the regulation of various cellular processes. The present review will, first, provide a general background on the molecular regulation of protein O-GlcNAcylation and will summarize the role of this post-translational modification in various acute cardiac pathologies including ischemia-reperfusion. Then, we will focus on research studies examining protein O-GlcNAcylation in the context of cardiac hypertrophy. A particular emphasis will be laid on the convergent but also divergent actions of O-GlcNAcylation according to the type of hypertrophy investigated, including physiological, pressure overload-induced and diabetes-linked cardiac hypertrophy. In an attempt to distinguish whether O-GlcNAcylation is detrimental or beneficial, this review will present the different O-GlcNAcylated targets involved in hypertrophy development. We will finally argue on potential interest to target O-GlcNAc processes to treat cardiac hypertrophy. This article is part of a Special Issue entitled: The role of post translational protein modifications on heart and vascular metabolism edited by Jason R.B. Dyck & Jan F.C. Glatz. (C) 2016 Elsevier B.V. All rights reserved.

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