Key result
The author raises concerns that testing lisinopril and spironolactone together in mdx mice prevents the analysis of the isolated antifibrotic effects of spironolactone.
Why the study?
Does early treatment with lisinopril and spironolactone preserve cardiac and skeletal muscle in Duchenne muscular dystrophy mice?
Does early treatment with lisinopril and spironolactone preserve cardiac and skeletal muscle in Duchenne muscular dystrophy mice?
Answers are grounded in this paper and cite their sources.
This letter highlights the need to differentiate the specific antifibrotic effects of spironolactone from ACE inhibitors in Duchenne muscular dystrophy mouse models.
I read with great interest the article by Rafael-Fortney et al 1 about the effect of early treatment with lisinopril and spironolactone on cardiac and skeletal muscle in Duchenne muscular dystrophy mice. This article raised the concerns stated below. The authors have tested the 2 drugs lisinopril and spironolactone in utrn();mdx mice, and we cannot analyze the only effect of spironolactone. Bauer et al 2 demonstrated afterload reduction, lower end-systolic pressures in 16-week-old mdx mice treated with captopril, an angiotensin-converting enzyme inhibitor, during 8 weeks with an increase of the end-systolic elastance in the group mdx mice treated with captopril. Because no difference in fibrosis was noted in angiotensin-converting enzyme I group in comparison with untreated mice, we can postulate antifibrotic effects of spironolactone in Duchenne muscular dystrophy mice treated with spironolactone and angiotensin-converting enzyme inhibitors.
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Abdallah Fayssoil (2012) conducted a letter in Duchenne muscular dystrophy. Lisinopril and spironolactone was evaluated. The author raises concerns that testing lisinopril and spironolactone together in mdx mice prevents the analysis of the isolated antifibrotic effects of spironolactone.
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