Post-translational Modifications in Heart Failure: Small Changes, Big Impact

Heart Lung Circ. 2016 Apr;25(4):319-24. doi: 10.1016/j.hlc.2015.11.008. Epub 2015 Dec 4.

Abstract

Heart failure is a complex disease process with various aetiologies and is a significant cause of morbidity and death world-wide. Post-translational modifications (PTMs) alter protein structure and provide functional diversity in terms of physiological functions of the heart. In addition, alterations in protein PTMs have been implicated in human disease pathogenesis. Small ubiquitin-like modifier mediated modification (SUMOylation) pathway was found to play essential roles in cardiac development and function. Abnormal SUMOylation has emerged as a new feature of heart failure pathology. In this review, we will highlight the importance of SUMOylation as a regulatory mechanism of SERCA2a function, and its therapeutic potential for the treatment of heart failure.

Keywords: Heart failure; Post-translational modifications; SERCA2a; SUMO.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Heart Failure / metabolism*
  • Heart Failure / pathology
  • Heart Failure / therapy
  • Humans
  • Muscle Proteins / metabolism*
  • Myocardium / metabolism*
  • Myocardium / pathology
  • Sarcoplasmic Reticulum Calcium-Transporting ATPases / metabolism*
  • Sumoylation*

Substances

  • Muscle Proteins
  • Sarcoplasmic Reticulum Calcium-Transporting ATPases
  • ATP2A2 protein, human