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July 2, 2014Fibrogenesis & Tissue RepairOpen Access

HDAC class I inhibitor, Mocetinostat, reverses cardiac fibrosis in heart failure and diminishes CD90+ cardiac myofibroblast activation

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Why the study?

Does Mocetinostat reverse cardiac fibrosis and improve cardiac function in a rat model of ischemic heart failure?

Population

Rat model of congestive heart failure secondary to myocardial infarction created by left anterior descending…

Comparison

Mocetinostat administered for 3 weeks starting 3… vs Sham hearts and untreated CHF animals/cells

Design

Preclinical

Follow-up

6 weeks post MI (3 weeks of treatment)

Authors

HNHikmet Nural‐GuvenerBanner Sun Health Research InstituteLZLuidmila ZakharovaBanner HealthJNJames NimlosBanner Sun Health Research Institute

Discussion

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Implication

Preclinical support for class I HDAC inhibition in ischemic HF; leaves open translation to human trials.

Structured PICO

Does Mocetinostat reverse cardiac fibrosis and improve cardiac function in a rat model of ischemic heart failure?

P
Population
Rat model of congestive heart failure (CHF) secondary to myocardial infarction (MI) created by left anterior descending (LAD) coronary artery occlusion, and CD90+ fibroblasts isolated from atrial and ventricular heart tissue in vitro.
I
Intervention
Mocetinostat (selective class I HDAC inhibitor) administered for 3 weeks starting 3 weeks post-MI (in vivo) and applied to CD90+ cells (in vitro).
C
Comparator
Sham hearts and untreated CHF animals/cells
O
Outcome
Cardiac function (left ventricle end diastolic pressure and dp/dt max) and total collagen amount at 6 weeks post MIsurrogate

Selective class I HDAC inhibition with Mocetinostat reverses interstitial fibrosis and improves cardiac function in a rat model of ischemic heart failure.

Cite This Study

Nural‐Guvener et al. (2014) studied this question.

synapsesocial.com/papers/6a7646efb4bf63452708794dhttps://doi.org/10.1186/1755-1536-7-10
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