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Curcumin prevents and reverses murine cardiac hypertrophy

2008· article· en· 129 citations· W2115883095 on OpenAlex· 10.1172/jci32865

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Canadian affiliationAn author listed a Canadian institution. This is the only route the usual frame has.
Canadian funderA Canadian agency funded it. The work may carry no Canadian affiliation at all.

Post-publication record

Nature
Retraction
Reason
Duplication of/in Image;Error in Analyses;
Date
7/1/2009 0:00
Flagged by OpenAlex?
Yes

Source: Retraction Watch, joined by DOI. OpenAlex records retraction as is_retracted, a boolean over a state space with at least four values, so it cannot express an expression of concern, a correction or a reinstatement — it reports them as false, which reads as “fine”.

Abstract

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.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

The record

Venue
Journal of Clinical Investigation
Topic
Curcumin's Biomedical Applications
Field
Biochemistry, Genetics and Molecular Biology
Canadian institutions
University of ManitobaWestern UniversitySt. Boniface HospitalCanadian Institutes of Health ResearchHeart and Stroke FoundationToronto General HospitalUniversity of TorontoUniversity Health Network
Funders
Institute of Circulatory and Respiratory HealthCanadian Institutes of Health ResearchUniversity of TorontoUniversity of ManitobaHeart and Stroke Foundation of Canada
Keywords
CurcuminCardiac fibrosisMuscle hypertrophyFibrosisAcetylationHistoneP300-CBP Transcription FactorsChromatin remodelingBiologyEndocrinologyCancer researchInternal medicineChemistryPharmacologyMedicineHistone AcetyltransferasesBiochemistryGene
Has abstract in OpenAlex
yes