Therapeutic inhibition of miR-208a improves cardiac function and survival during heart failure.

ABSTRACT:

Background

Diastolic dysfunction in response to hypertrophy is a major clinical syndrome with few therapeutic options. MicroRNAs act as negative regulators of gene expression by inhibiting translation or promoting degradation of target mRNAs. Previously, we reported that genetic deletion of the cardiac-specific miR-208a prevents pathological cardiac remodeling and upregulation of Myh7 in response to pressure overload. Whether this miRNA might contribute to diastolic dysfunction or other forms of heart disease is currently unknown.

Methods and results

Here, we show that systemic delivery of an antisense oligonucleotide induces potent and sustained silencing of miR-208a in the heart. Therapeutic inhibition of miR-208a by subcutaneous delivery of antimiR-208a during hypertensio

SUBMITTER: Montgomery RL 

PROVIDER: S-EPMC3353551 | biostudies-literature | 2011 Oct

REPOSITORIES: biostudies-literature