Post‐translational modifications of the cardiac proteome in diabetes and heart failure

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 of 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 PTMs contributing to cardiovascular disease progression. PTMs 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 PTMs are involved in each of these pathways, we will highlight the role of the serine and threonine O‐linked addition of β‐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.

Location
Deutsche Nationalbibliothek Frankfurt am Main
Extent
Online-Ressource
Language
Englisch

Bibliographic citation
Post‐translational modifications of the cardiac proteome in diabetes and heart failure ; volume:10 ; number:1 ; year:2016 ; pages:25-38 ; extent:14
Proteomics / Clinical applications. Clinical applications ; 10, Heft 1 (2016), 25-38 (gesamt 14)

Creator
Wende, Adam R.

DOI
10.1002/prca.201500052
URN
urn:nbn:de:101:1-2022111905083768097466
Rights
Open Access; Der Zugriff auf das Objekt ist unbeschränkt möglich.
Last update
15.08.2025, 7:23 AM CEST

Data provider

This object is provided by:
Deutsche Nationalbibliothek. If you have any questions about the object, please contact the data provider.

Associated

  • Wende, Adam R.

Other Objects (12)