ArticleCell death & disease2022
GCN5-mediated regulation of pathological cardiac hypertrophy via activation of the TAK1-JNK/p38 signaling pathway.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- METTL7B attenuates pathological cardiac hypertrophy via m6A-associated regulation of HK3.Molecular and cellular biochemistry · 2026Article
- A succinylation-based classifier predicts chemotherapy response in prostate cancer and reveals KAT2A as a therapeutic target.Clinical and translational medicine · 2026Article
- Loss of p300/CBP-associated factor aggravates cardiac remodeling via regulation of CAMKK2 acetylation.Experimental & molecular medicine · 2026Article
- ABCC9 knockdown attenuates isoproterenol‑induced myocardial hypertrophy by inhibiting the PI3K/AKT signaling pathway.Molecular medicine reports · 2026Article
- FTO-Eci1 Axis Mediates Exercise-Induced Cardioprotection in Pressure Overload Mice.Biomolecules · 2026Article
- Research progress of OTUD7B: from structural function and disease mechanisms to clinical translation.Frontiers in immunology · 2026Review
- RBM25 Regulates p38 MAPK Pathway Activation via Exon 16 Skipping of MAP4K4 in a Rat Model of Post-Infarction Heart Failure.FASEB bioAdvances · 2025Article
- Loss of PCAF in proximal tubular cells exacerbates renal fibrosis by promoting partial epithelial-to-mesenchymal transition.Experimental & molecular medicine · 2025Article
- Integrative Mendelian randomization and multi-omics analysis identifies anti-allergic drug targets associated with cardiovascular disease risk.Scientific reports · 2025Article
- TSH upregulates CYP4B1 through the PI3K/AKT/CREB pathway to promote cardiac hypertrophy.Journal of endocrinological investigation · 2025Article
- Implications of Quercetin in Mitigating Myocardial Ischemia-Reperfusion Injury: A Review Study.Advanced biomedical research · 2025Review
- Fas Apoptosis Inhibitory Molecule 2 Inhibits Pathological Cardiac Hypertrophy by Regulating the MAPK Signaling Pathway.Journal of the American Heart Association · 2024Article
- KAT2A and KAT2B prevent double-stranded RNA accumulation and interferon signaling to maintain intestinal stem cell renewal.Science advances · 2024Article
- Lactate regulates pathological cardiac hypertrophy via histone lactylation modification.Journal of cellular and molecular medicine · 2024Article
- Histone acetyltransferase Kat2a regulates ferroptosis via enhancing Tfrc and Hmox1 expression in diabetic cardiomyopathy.Cell death & disease · 2024Article
- The role of deubiquitinases in cardiac disease.Expert reviews in molecular medicine · 2024Review
- The Potential Therapeutic Prospect of PANoptosis in Heart Failure.Journal of inflammation research · 2024Review
- TBC1 domain family member 25 protects against myocardial apoptosis and the proinflammatory response triggered by ischemia-reperfusion injury through suppression of the TAK1-JNK/p38 MAPK signaling cascade.In vitro cellular & developmental biology. Animal · 2023Article
- Transforming growth factor-β and bone morphogenetic protein signaling pathways in pathological cardiac hypertrophy.Cell cycle (Georgetown, Tex.) · 2023Review
- FGF21-FGFR1 controls mitochondrial homeostasis in cardiomyocytes by modulating the degradation of OPA1.Cell death & disease · 2023Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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