Key result
Right ventricular hypertrophy in pediatric heart surgery linked to increased HO-1 and HSP70 expression in ~100% of specimens.
Why the study?
Reactive oxygen species are implicated in cardiac hypertrophy, and haem oxygenase-1 (HO-1) is induced by oxidative stress to protect against tissue injury, motivating examination of HO-1 and heat shock protein 70 (HSP70) expression in hypertrophic myocardium.
Observational (n=8)
Hypertrophic right ventricular myocardium in pediatric congenital heart disease patients exhibits significant, separately regulated upregulation of stress-response genes HO-1 and HSP70.
Answers are grounded in this paper and cite their sources.
Potential protective role of HO-1 in pediatric cardiac hypertrophy is hypothesis-generating; leaves open any clinical relevance in congenital heart disease.
Reactive oxygen species are implicated in the pathogenesis of cardiac hypertrophy. Haem oxygenase-1 (HO-1), the rate-limiting enzyme in haem catabolism, is induced by oxidative stress and confers protection against oxidative tissue injuries. We used Northern blotting to examine expression of HO-1 and heat shock protein 70 (HSP70) in the hypertrophic cardiac muscle of eight patients (one infant and seven children) who underwent surgery for congenital heart disease. Levels of HO-1 and HSP70 mRNA were significantly increased in all specimens, but the orders of magnitude of the increases were different, suggesting that the genes expressing HO-1 and HSP70 are regulated separately.
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Takeuchi et al. (2003) conducted an observational in Congenital heart disease with cardiac hypertrophy (n=8). Congenital heart disease / cardiac hypertrophy was evaluated on mRNA expression levels of haem oxygenase-1 (HO-1) and heat shock protein 70 (HSP70) in right ventricular muscle. Hypertrophic right ventricular muscle in 8 children undergoing congenital cardiac surgery showed significantly increased HO-1 and HSP70 mRNA in 100% (8/8) of specimens.
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