MicroRNA-133 controls cardiac hypertrophy

Alessandra Carè, Daniele Catalucci, Federica Felicetti, Désirée Bonci, Antonio Addario, Paolo Gallo, Marie Louise Bang, Patrizia Segnalini, Yusu Gu, Nancy D. Dalton, Leonardo Elia, Michael V.G. Latronico, Morten Høydal, Camillo Autore, Matteo A. Russo, Gerald W. Dorn, Øyvind Ellingsen, Pilar Ruiz-Lozano, Kirk L. Peterson, Carlo M. CroceCesare Peschle, Gianluigi Condorelli

Research output: Contribution to journalArticlepeer-review

1551 Scopus citations


Growing evidence indicates that microRNAs (miRNAs or miRs) are involved in basic cell functions and oncogenesis. Here we report that miR-133 has a critical role in determining cardiomyocyte hypertrophy. We observed decreased expression of both miR-133 and miR-1, which belong to the same transcriptional unit, in mouse and human models of cardiac hypertrophy. In vitro overexpression of miR-133 or miR-1 inhibited cardiac hypertrophy. In contrast, suppression of miR-133 by 'decoy' sequences induced hypertrophy, which was more pronounced than that after stimulation with conventional inducers of hypertrophy. In vivo inhibition of miR-133 by a single infusion of an antagomir caused marked and sustained cardiac hypertrophy. We identified specific targets of miR-133: RhoA, a GDP-GTP exchange protein regulating cardiac hypertrophy; Cdc42, a signal transduction kinase implicated in hypertrophy; and Nelf-A/WHSC2, a nuclear factor involved in cardiogenesis. Our data show that miR-133, and possibly miR-1, are key regulators of cardiac hypertrophy, suggesting their therapeutic application in heart disease.

Original languageEnglish
Pages (from-to)613-618
Number of pages6
JournalNature medicine
Issue number5
StatePublished - May 2007


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