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Curcumin prevents and reverses murine cardiac hypertrophy.

Authors: Li, HL  Liu, C  De Couto, G  Ouzounian, M  Sun, M  Wang, AB  Huang, Y  He, CW  Shi, Y  Chen, X  Nghiem, MP  Liu, Y  Chen, M  Dawood, F  Fukuoka, M  Maekawa, Y  Zhang, L  Leask, A  Ghosh, AK  Kirshenbaum, LA  Liu, PP 
Citation: Li HL, etal., J Clin Invest. 2008 Mar;118(3):879-93.
Pubmed: (View Article at PubMed) PMID:18292803
DOI: Full-text: DOI:10.1172/JCI32865

Chromatin remodeling, particularly histone acetylation, plays a critical role in the progression of pathological cardiac hypertrophy and heart failure. We hypothesized that curcumin, a natural polyphenolic compound abundant in the spice turmeric and a known suppressor of histone acetylation, would suppress cardiac hypertrophy through the disruption of p300 histone acetyltransferase-dependent (p300-HAT-dependent) transcriptional activation. We tested this hypothesis using primary cultured rat cardiac myocytes and fibroblasts as well as two well-established mouse models of cardiac hypertrophy. Curcumin blocked phenylephrin-induced (PE-induced) cardiac hypertrophy in vitro in a dose-dependent manner. Furthermore, curcumin both prevented and reversed mouse cardiac hypertrophy induced by aortic banding (AB) and PE infusion, as assessed by heart weight/BW and lung weight/BW ratios, echocardiographic parameters, and gene expression of hypertrophic markers. Further investigation demonstrated that curcumin abrogated histone acetylation, GATA4 acetylation, and DNA-binding activity through blocking p300-HAT activity. Curcumin also blocked AB-induced inflammation and fibrosis through disrupting p300-HAT-dependent signaling pathways. Our results indicate that curcumin has the potential to protect against cardiac hypertrophy, inflammation, and fibrosis through suppression of p300-HAT activity and downstream GATA4, NF-kappaB, and TGF-beta-Smad signaling pathways.

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CRRD Object Information
CRRD ID: 2312266
Created: 2009-08-03
Species: All species
Last Modified: 2009-08-03
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.