期刊
HEART LUNG AND CIRCULATION
卷 25, 期 4, 页码 319-324出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.hlc.2015.11.008
关键词
Heart failure; Post-translational modifications; SUMO; SERCA2a
资金
- NIH [R00 HL116645, R01 HL117505, HL093183, P50 HL112324]
- NHLBI Program of Excellence in Nanotechnology (PEN) Award [HHSN268201000045C]
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.
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