ArticleNaunyn-Schmiedeberg's archives of pharmacology2009
Differential roles of nitric oxide synthase isozymes in cardiotoxicity and mortality following chronic doxorubicin treatment in mice.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
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Who cites it
16 citing papers in PubMed, 35 citations in OpenAlex.
- Polymorphisms of ABCC5 and NOS3 genes influence doxorubicin cardiotoxicity in survivors of childhood acute lymphoblastic leukemia.The pharmacogenomics journal · 2016Trial
- Review
- NO/NOS system dysregulation as a key molecular mechanism in chemotherapy-induced cardiotoxicity: a review.Frontiers in cardiovascular medicine · 2025Review
- Ursolic acid prevents doxorubicin-induced cardiac toxicity in mice through eNOS activation and inhibition of eNOS uncoupling.Journal of cellular and molecular medicine · 2019Article
- Pristimerin protects against doxorubicin-induced cardiotoxicity and fibrosis through modulation of Nrf2 and MAPK/NF-kB signaling pathways.Cancer management and research · 2019Article
- Aldose reductase inhibitor, fidarestat prevents doxorubicin-induced endothelial cell death and dysfunction.Biochemical pharmacology · 2018Article
- Cardiac spheroids as promising in vitro models to study the human heart microenvironment.Scientific reports · 2017Article
- Arginine-Nitric Oxide Metabolites and Cardiac Dysfunction in Patients With Breast Cancer.Journal of the American College of Cardiology · 2017Article
- microRNAs and Acute Myeloid Leukemia Chemoresistance: A Mechanistic Overview.Frontiers in oncology · 2017Review
- Testosterone Antagonizes Doxorubicin-Induced Senescence of Cardiomyocytes.Journal of the American Heart Association · 2016Article
- The role of nitric oxide in Doxorubicin-induced cardiotoxicity: experimental study.Turkish journal of haematology : official journal of Turkish Society of Haematology · 2014Article
- HBOC vasoactivity: interplay between nitric oxide scavenging and capacity to generate bioactive nitric oxide species.Antioxidants & redox signaling · 2013Review
- Oxidative stress, redox signaling, and metal chelation in anthracycline cardiotoxicity and pharmacological cardioprotection.Antioxidants & redox signaling · 2013Review
- Dietary inorganic nitrate alleviates doxorubicin cardiotoxicity: mechanisms and implications.Nitric oxide : biology and chemistry · 2012Review
- Chronic cardiotoxicity of doxorubicin involves activation of myocardial and circulating matrix metalloproteinases in rats.Acta pharmacologica Sinica · 2012Article
- Developing a rat model of dilated cardiomyopathy with improved survival.Journal of Zhejiang University. Science. BArticle
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The roles of individual nitric oxide synthases (NOS) in anthracycline-related cardiotoxicity are not completely understood. We investigated the effects of a chronic treatment with doxorubicin (DOX) on knockouts of the individual NOS isozymes and on transgenic mice with myocardial overexpression of eNOS. Fractional shortening (FS) was reduced in untreated homozygous nNOS and iNOS knockouts as well as in eNOS transgenics. DOX-induced FS decrease in wild-type mice was attenuated only in eNOS knockouts, which were found to overexpress nNOS. No worsening of contractility was observed in DOX-treated eNOS transgenics and iNOS knockouts. Although the surviving DOX-treated nNOS knockouts exhibited no further impairment in contractility, most (70%) animals died within 7 weeks after treatment onset. In comparison to untreated wild-type hearts, the nitric oxide (NO) level was lower in hearts from DOX-treated wild-type mice and in all three untreated knockouts. DOX treatment had no effect on NO in the knockouts. These data indicate differential roles of the individual NOS in DOX-induced cardiotoxicity. Protection against DOX effects conferred by eNOS deletion may be mediated by a compensatory overexpression of nNOS. NOS inhibition-based prevention of anthracycline-induced cardiotoxicity should be eNOS-selective, simultaneously avoiding inhibiting nNOS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.