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Curcumin prevents and reverses murine cardiac hypertrophy
Li H.-L.1; Liu C.1; De Couto G.1; Ouzounian M.1; Sun M.1; Wang A.-B.2; Huang Y.3; He C.-W.4; Shi Y.1; Chen X.1; Nghiem M.P.1; Liu Y.1; Chen M.1; Dawood F.1; Fukuoka M.1; Maekawa Y.1; Zhang L.1; Leask A.5; Ghosh A.K.6; Kirshenbaum L.A.7; Liu P.P.1,8
Source PublicationJournal of Clinical Investigation
ISSN00219738 15588238

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-κB, and TGF-β-Smad signaling pathways.

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Indexed BySCI
WOS Research AreaResearch & Experimental Medicine
WOS SubjectMedicine, Research & Experimental
WOS IDWOS:000267694300038
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Cited Times [WOS]:1   [WOS Record]     [Related Records in WOS]
Document TypeJournal article
CollectionInstitute of Chinese Medical Sciences
Affiliation1.Division of Cardiology, Heart and Stroke/Richard Lewar Centre of Excellence, University Health Network, University of Toronto, Toronto, Ontario, Canada.
2.Laboratory of Molecular Cardiology, National Heart, Lung, and Blood Institute, NIH, Bethesda, Maryland, USA.
3.Wellcome Trust Genome Campus and Sanger Institute, Hinxton, Cambridge, United Kingdom.
4.Department of Medicine, Massachusetts General Hospital, and Harvard Medical School, Boston, Massachusetts, USA.
5.Division of Oral Biology and Department of Physiology and Pharmacology, Canadian Institutes of Health Research (CIHR) Group in Skeletal Development and Remodeling, Schulich School of Medicine and Dentistry, University of Western Ontario, London, Ontario, Canada.
6.Division of Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
7.Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Winnipeg, Manitoba, Canada.
8.Institute of Circulatory and Respiratory Health, Canadian Institutes of Health Research, Ottawa, Ontario, Canada.
Recommended Citation
GB/T 7714
Li H.-L.,Liu C.,De Couto G.,et al. Curcumin prevents and reverses murine cardiac hypertrophy[J]. Journal of Clinical Investigation,2008,118(3):879-893.
APA Li H.-L..,Liu C..,De Couto G..,Ouzounian M..,Sun M..,...&Liu P.P..(2008).Curcumin prevents and reverses murine cardiac hypertrophy.Journal of Clinical Investigation,118(3),879-893.
MLA Li H.-L.,et al."Curcumin prevents and reverses murine cardiac hypertrophy".Journal of Clinical Investigation 118.3(2008):879-893.
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