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GCN5-mediated regulation of pathological cardiac hypertrophy via activation of the TAK1-JNK/p38 signaling pathway

Cell death & disease, 2022-04, Vol.13 (4), p.421-421, Article 421 [Peer Reviewed Journal]

2022. The Author(s). ;The Author(s) 2022. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. ;The Author(s) 2022 ;ISSN: 2041-4889 ;EISSN: 2041-4889 ;DOI: 10.1038/s41419-022-04881-y ;PMID: 35490166

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Title:
GCN5-mediated regulation of pathological cardiac hypertrophy via activation of the TAK1-JNK/p38 signaling pathway
Author: Li, Jia ; Yan, Chenghui ; Wang, Yilong ; Chen, Can ; Yu, Haibo ; Liu, Dan ; Huang, Kai ; Han, Yaling
Subjects: Animals ; Aorta ; c-Jun protein ; Cardiomegaly - metabolism ; Cardiomyocytes ; Congestive heart failure ; Histone acetyltransferase ; Histone Acetyltransferases - metabolism ; Humans ; Hypertrophy ; JNK protein ; Kinases ; Lysine ; Lysine Acetyltransferases - metabolism ; MAP Kinase Kinase Kinases - metabolism ; MAP Kinase Signaling System ; Mice ; Morbidity ; Myocytes, Cardiac - metabolism ; Neonates ; p300-CBP Transcription Factors - metabolism ; Phenylephrine ; Rats ; Risk factors ; Signal Transduction ; TAK1 protein ; Transcription factors ; Transforming growth factor-b
Is Part Of: Cell death & disease, 2022-04, Vol.13 (4), p.421-421, Article 421
Description: Pathological cardiac hypertrophy is a process of abnormal remodeling of cardiomyocytes in response to pressure overload or other stress stimuli, resulting in myocardial injury, which is a major risk factor for heart failure, leading to increased morbidity and mortality. General control nonrepressed protein 5 (GCN5)/lysine acetyltransferase 2 A, a member of the histone acetyltransferase and lysine acetyltransferase families, regulates a variety of physiological and pathological events. However, the function of GCN5 in pathological cardiac hypertrophy remains unclear. This study aimed to explore the role of GCN5 in the development of pathological cardiac hypertrophy. GCN5 expression was increased in isolated neonatal rat cardiomyocytes (NRCMs) and mouse hearts of a hypertrophic mouse model. GCN5 overexpression aggravated the cardiac hypertrophy triggered by transverse aortic constriction surgery. In contrast, inhibition of GCN5 impairs the development of pathological cardiac hypertrophy. Similar results were obtained upon stimulation of NRCMs (having GCN5 overexpressed or knocked down) with phenylephrine. Mechanistically, our results indicate that GCN5 exacerbates cardiac hypertrophy via excessive activation of the transforming growth factor β-activated kinase 1 (TAK1)-c-Jun N-terminal kinase (JNK)/p38 signaling pathway. Using a TAK1-specific inhibitor in rescue experiments confirmed that the activation of TAK1 is essential for GCN5-mediated cardiac hypertrophy. In summary, the current study elucidated the role of GCN5 in promotion of cardiac hypertrophy, thereby implying it to be a potential target for treatment.
Publisher: England: Springer Nature B.V
Language: English
Identifier: ISSN: 2041-4889
EISSN: 2041-4889
DOI: 10.1038/s41419-022-04881-y
PMID: 35490166
Source: Open Access: Nature Open Access
AUTh Library subscriptions: ProQuest Central
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GCN5-mediated regulation of pathological cardiac hypertrophy via activation of the TAK1-JNK/p38 signaling pathway

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