ArticleExperimental biology and medicine (Maywood, N.J.)2009
Heme oxygenase-1 inhibits pro-oxidant induced hypertrophy in HL-1 cardiomyocytes.
Article in Experimental biology and medicine (Maywood, N.J.), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 37 citations in OpenAlex.
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- Porous, Ventricular Extracellular Matrix-Derived Foams as a Platform for Cardiac Cell Culture.BioResearch open access · 2015Article
- Cardiac thromboxane A2 receptor activation does not directly induce cardiomyocyte hypertrophy but does cause cell death that is prevented with gentamicin and 2-APB.BMC pharmacology & toxicology · 2014Article
- Dystrophic muscle improvement in zebrafish via increased heme oxygenase signaling.Human molecular genetics · 2014Article
- FGF23 is a novel regulator of intracellular calcium and cardiac contractility in addition to cardiac hypertrophy.American journal of physiology. Endocrinology and metabolism · 2013Article
- Anti-Proliferative Effect of an Aqueous Extract of Prunella vulgaris in Vascular Smooth Muscle Cells.Evidence-based complementary and alternative medicine : eCAM · 2013Article
- Store-operated calcium entry is present in HL-1 cardiomyocytes and contributes to resting calcium.Biochemical and biophysical research communications · 2011Article
- The coordinated increased expression of biliverdin reductase and heme oxygenase-2 promotes cardiomyocyte survival: a reductase-based peptide counters β-adrenergic receptor ligand-mediated cardiac dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2011Article
- Equilibrative nucleoside transporter 1 plays an essential role in cardioprotection.American journal of physiology. Heart and circulatory physiology · 2010Article
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
aimsReactive oxygen species (ROS) activate multiple signaling pathways involved in cardiac hypertrophy. Since HO-1 exerts potent antioxidant effects, we hypothesized that this enzyme inhibits ROS-induced cardiomyocyte hypertrophy.
methodsHL-1 cardiomyocytes were transduced with an adenovirus constitutively expressing HO-1 (AdHO-1) to increase basal HO-1 expression and then exposed to 200 microM hydrogen peroxide (H2O2). Hypertrophy was measured using 3H-leucine incorporation, planar morphometry and cell-size by forward-scatter flow-cytometry. The pro-oxidant effect of H2O2 was assessed by redox sensitive fluorophores. Inducing intracellular redox imbalance resulted in cardiomyocyte hypertrophy through transactivation of nuclear factor kappa B (NF-kappaB).
resultsPre-emptive HO-1 overexpression attenuated the redox imbalance and reduced hypertrophic indices. This is the first time that HO-1 has directly been shown to inhibit oxidant-induced cardiomyocyte hypertrophy by a NF-kappaB-dependent mechanism.
conclusionThese results demonstrate that HO-1 inhibits pro-oxidant induced cardiomyocyte hypertrophy and suggest that HO-1 may yield therapeutic potential in treatment of.
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