The role of post‐translational modifications in cardiac hypertrophy

Pathological cardiac hypertrophy involves excessive protein synthesis, increased cardiac myocyte size and ultimately the development of heart failure. Thus, pathological cardiac hypertrophy is a major risk factor for many cardiovascular diseases and death in humans. Extensive research in the last de...

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Bibliographic Details
Published in:Journal of cellular and molecular medicine 2019-06, Vol.23 (6), p.3795-3807
Main Authors: Yan, Kaowen, Wang, Kun, Li, Peifeng
Format: Article
Language:English
Subjects:
Acetylation
Acetylglucosamine - metabolism
Animals
cardiac hypertrophy
Cardiomegaly - genetics
Cardiomegaly - metabolism
Dual-Specificity Phosphatases - genetics
Dual-Specificity Phosphatases - metabolism
heart failure
Histone Deacetylases - genetics
Histone Deacetylases - metabolism
Humans
Methylation
Myocytes, Cardiac - chemistry
Myocytes, Cardiac - metabolism
Phosphorylation
post‐translational modifications (PTMs)
Protein Processing, Post-Translational
Review
Reviews
Signal Transduction
Sumoylation
Ubiquitin-Protein Ligases - genetics
Ubiquitin-Protein Ligases - metabolism
Ubiquitination
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Summary:Pathological cardiac hypertrophy involves excessive protein synthesis, increased cardiac myocyte size and ultimately the development of heart failure. Thus, pathological cardiac hypertrophy is a major risk factor for many cardiovascular diseases and death in humans. Extensive research in the last decade has revealed that post‐translational modifications (PTMs), including phosphorylation, ubiquitination, SUMOylation, O‐GlcNAcylation, methylation and acetylation, play important roles in pathological cardiac hypertrophy pathways. These PTMs potently mediate myocardial hypertrophy responses via the interaction, stability, degradation, cellular translocation and activation of receptors, adaptors and signal transduction events. These changes occur in response to pathological hypertrophy stimuli. In this review, we summarize the roles of PTMs in regulating the development of pathological cardiac hypertrophy. Furthermore, PTMs are discussed as potential targets for treating or preventing cardiac hypertrophy.
ISSN:1582-1838
1582-4934
DOI:10.1111/jcmm.14330