Heart failure: targeting transcriptional and post-transcriptional control mechanisms of hypertrophy for treatment.
Heart failure (HF) is a syndrome caused by diminished heart function that arises from pathologies like hypertension, infarction, and diabetes. Neurohormonal, cardiorenal and cardiocirculatory models have been developed to explain HF but they have not provided sufficient understanding for the elaboration of therapies to conquer the syndrome. In fact, even though progress has been made in improving survival, HF remains a frequent cause of hospitalization and death. Since in most forms of HF, development of the disorder is associated with an alteration of cardiomyocyte structure, perceived as an increase in heart mass due to cell hypertrophy, effort is being directed to address hypertrophy as a therapeutic target. Here, we outline recent understanding of two gene-silencing regulatory mechanisms underlying cardiomyocyte hypertrophy, i.e., transcriptional control by HDACs, and post-transcriptional control by microRNAs.
Laboratory of Molecular Cardiology, Scientific and Technology Pole, IRCCS MultiMedica Hospital, 20138 Milan, Italy.
Michael V G
MV
Latronico
Leonardo
L
Elia
Gianluigi
G
Condorelli
Daniele
D
Catalucci
D000818:Animals; D006332:Cardiomegaly / Q000235:genetics* / Q000378:metabolism; D006333:Heart Failure / Q000188:drug therapy* / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D006655:Histone Deacetylases / Q000378:metabolism; D006801:Humans; D035683:MicroRNAs / Q000378:metabolism; D012323:RNA Processing, Post-Transcriptional; D014158:Transcription, Genetic
D035683:MicroRNAs; D006655:Histone Deacetylases