Why the study?
Does miR29b expression change in AF/CHF and does its modulation affect atrial fibrotic remodeling?
Population
Animal models, canine atrial fibroblasts, and human patients with atrial fibrillation and/or congestive…
Comparison
Ventricular tachypacing; lentivirus-mediated… vs Control dogs; empty virus-infected fibroblasts…
Design
Preclinical
Follow-up
Up to 2 weeks (in dog model)
Authors
Discussion
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Implication
MiR29b may inform biomarker or target development in AF/CHF; hypothesis-generating from Level 5 data, human trials needed.
Structured PICO
Does miR29b expression change in AF/CHF and does its modulation affect atrial fibrotic remodeling?
P
Population
Animal models (dogs subjected to ventricular tachypacing, mice), canine atrial fibroblasts, and human patients with atrial fibrillation (AF) and/or congestive heart failure (CHF).
I
Intervention
Ventricular tachypacing (dogs); lentivirus-mediated miR29b knockdown or overexpression (fibroblasts); adenoassociated viral-mediated knockdown of miR29b (mice).
C
Comparator
Control dogs; empty virus-infected fibroblasts or scrambled control; patients in sinus rhythm or without CHF/AF.
O
Outcome
miR29b expression levels and expression of extracellular matrix target genes (COL1A1, COL3A1, fibrillin).surrogate
MiR29b is downregulated in CHF and AF, and its modulation directly affects atrial fibrotic remodeling, suggesting potential as a biomarker or therapeutic target.
Cite This Study
Dawson et al. (2013) studied this question.