February 1, 2007Journal of Molecular Endocrinology
Npr1-regulated gene pathways contributing to cardiac hypertrophy and fibrosis
Population
Male and female Npr1 knockout mice (Npr1-/-) at 8 weeks and 6 months of age
Comparison
Npr1 gene knockout (lack of Npr1 signalling) vs Wild-type (WT) mice
Design
Preclinical
Follow-up
8 weeks and 6 months of age
Authors
Discussion
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Implication
Highlights candidate hypertrophy pathways in Npr1 deficiency; hypothesis-generating in mice and should not change practice.
Structured PICO
P
Population
Male and female Npr1 knockout mice (Npr1-/-) at 8 weeks and 6 months of age
I
Intervention
Npr1 gene knockout (lack of Npr1 signalling)
C
Comparator
Wild-type (WT) mice
O
Outcome
Gene expression alterations in hypertrophic and fibrotic pathways (measured by cDNA microarray and RT-PCR), heart weight to body weight ratios (HW:BW), and blood pressuresurrogate
The study identifies the calmodulin-CaMK-Hdac-Mef2 and PKC-MAPK-GATA4 pathways as key mediators of cardiac hypertrophy in the absence of Npr1 signaling.
Cite This Study
Ellmers et al. (2007) studied this question.