Post-translational modifications of the cardiac proteome in diabetes and heart
failure.
Authors Wende AR
Submitted By Adam Wende on 7/7/2015
Status Published
Journal Proteomics. Clinical applications
Year 2015
Date Published 7/3/2015
Volume : Pages Not Specified : Not Specified
PubMed Reference 26140508
Abstract Cardiovascular complications are the leading cause of death in diabetic
patients. Decades of research has focused on altered gene expression, altered
cellular signaling, and altered metabolism. This work has led to better
understanding disease progression and treatments aimed at reversing or stopping
this deadly process. However, one of the pieces needed to complete the puzzle
and bridge the gap between altered gene expression and changes in
signaling/metabolism is the proteome and its host of modifications. Defining the
mechanisms of regulation includes examining protein levels, localization, and
activity of the functional component of cellular machinery. Excess or
misutilization of nutrients in obesity and diabetes may lead to
post-translational modifications contributing to cardiovascular disease
progression. Post-translational modifications link regulation of metabolic
changes in the healthy and diseased heart with regulation of gene expression
itself (e.g. epigenetics), protein enzymatic activity (e.g. mitochondrial
oxidative capacity), and function (e.g. contractile machinery). Although a
number of post-translational modifications are involved in each of these
pathways, we will highlight the role of the serine and threonine O-linked
addition of ß-N-acetyl-glucosamine or O-GlcNAcylation. This nexus of nutrient
supply, utilization, and storage allows for the modification and translation of
mitochondrial function to many other aspects of the cell. This article is
protected by copyright. All rights reserved.


Investigators with authorship
NameInstitution
Adam WendeUniversity of Alabama at Birmingham

Complications