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

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

Ahyoung Lee  1 , Jae Gyun Oh  1 , Przemek A Gorski  1 , Roger J Hajjar  1 , Changwon Kho  2
Affiliations
Review

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

Ahyoung Lee et al. Heart Lung Circ. 2016 Apr.

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.

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Figures

FIGURE 1
FIGURE 1. SUMOylation of SERCA2a in the heart as a therapeutic target
The impaired myocardial SERCA2a expression and its activity are a signature of heart failure. In the failing heart, SERCA2a SUMOylation is reduced due to a decrease in SUMO1 expression. We propose that SERCA2a dysfunction can be restored by either (i) gene delivery mediated SUMO1 overexpression or (ii) small molecule activation of SUMOylation enzymes, both of which can increase SERCA2a SUMOylation and may present as novel therapeutic approaches for the treatment of heart failure. SERCA2a; sarcoplasmic/endoplasmic reticulum Ca2+-ATPase 2a, SUMO1; small ubiquitin like modifier 1
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References

    1. Bui AL, Horwich TB, Fonarow GC. Epidemiology and risk profile of heart failure. Nature Reviews Cardiology. 2011;8:30–41. - PMC - PubMed
    1. Mosterd A, Hoes AW. Clinical epidemiology of heart failure. Heart. 2007;93:1137–46. - PMC - PubMed
    1. Go AS, Mozaffarian D, Roger VL, Benjamin EJ, Berry JD, Blaha MJ, et al. Heart disease and stroke statistics--2014 update: a report from the American Heart Association. Circulation. 2014;129:e28–e292. - PMC - PubMed
    1. Jhund PS, Macintyre K, Simpson CR, Lewsey JD, Stewart S, Redpath A, et al. Long-term trends in first hospitalization for heart failure and subsequent survival between 1986 and 2003: a population study of 5.1 million people. Circulation. 2009;119:515–23. - PubMed
    1. Raymer B, Ebner D. Small molecule and peptide therapies for chronic heart failure: a patent review (2011 -2014). Expert Opinion on Therapeutic Patents. 2015:1–16. - PubMed

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