Key result
Androgen receptor knockout in male mice significantly reduced the heart-to-body weight ratio and exacerbated Angiotensin II-induced cardiac fibrosis and left ventricular dysfunction.
Why the study?
Does the androgen-nuclear androgen receptor (AR) system contribute to cardiac growth and angiotensin II-stimulated cardiac remodeling in male mice?
Population
25-week-old systemic androgen receptor knock-out (ARKO) male mice and age-matched wild-type (WT) male mice
Comparison
Angiotensin II stimulation for 2 weeks vs Without Ang II stimulation, and wild-type mice
Design
Preclinical
Follow-up
2 weeks
Authors
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AR signaling supports male cardiac growth and limits fibrosis under stress; leaves open translation to human remodeling therapies.
Does the androgen-nuclear androgen receptor (AR) system contribute to cardiac growth and angiotensin II-stimulated cardiac remodeling in male mice?
The androgen-androgen receptor system plays a role in normal cardiac growth and modulates adaptive hypertrophy and fibrosis during cardiac remodeling under hypertrophic stress in male mice.
Ikeda et al. (2005) studied Cardiac growth and Angiotensin II-induced cardiac fibrosis. Androgen receptor gene knockout (ARKO) and Angiotensin II stimulation vs. Wild-type (WT) male mice was evaluated on Heart-to-body weight ratio, cardiac hypertrophy, left ventricular function, and cardiac fibrosis. Androgen receptor knockout in male mice significantly reduced the heart-to-body weight ratio and exacerbated Angiotensin II-induced cardiac fibrosis and left ventricular dysfunction.