ArticleTheScientificWorldJournal2012
Activation of β-adrenoceptors by dobutamine may induce a higher expression of peroxisome proliferator-activated receptors δ (PPARδ) in neonatal rat cardiomyocytes.
Article in TheScientificWorldJournal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Istaroxime in Acute Heart Failure and Early Cardiogenic Shock: A Calcium-Cycling Approach to Inotropic Therapy.International journal of molecular sciences · 2026Review
- Ginseng in white and red processed forms: Ginsenosides and cardiac side effects.Food science & nutrition · 2024Article
- Roles of distinct nuclear receptors in diabetic cardiomyopathy.Frontiers in pharmacology · 2024Review
- CODA: Integrating multi-level context-oriented directed associations for analysis of drug effects.Scientific reports · 2017Article
- Preventive and therapeutic effects of a beta adrenoreceptor agonist, dobutamine, in carrageenan-induced inflammatory nociception in rats.Inflammation · 2014Article
- Merit of ginseng in the treatment of heart failure in type 1-like diabetic rats.BioMed research international · 2014Article
- Ginseng is useful to enhance cardiac contractility in animals.BioMed research international · 2014Article
- Doxorubicin-Induced Cardiac Toxicity Is Mediated by Lowering of Peroxisome Proliferator-Activated Receptor δ Expression in Rats.PPAR research · 2013Article
- Cardiac peroxisome proliferator-activated receptor δ (PPARδ) as a new target for increased contractility without altering heart rate.PloS one · 2013Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent evidence showed the role of peroxisome proliferator-activated receptors (PPARs) in cardiac function. Cardiac contraction induced by various agents is critical in restoring the activity of peroxisome proliferator-activated receptors δ (PPARδ) in cardiac myopathy. Because dobutamine is an agent widely used to treat heart failure in emergency setting, this study is aimed to investigate the change of PPARδ in response to dobutamine. Neonatal rat cardiomyocytes were used to examine the effects of dobutamine on PPARδ expression levels and cardiac troponin I (cTnI) phosphorylation via Western blotting analysis. We show that treatment with dobutamine increased PPARδ expression and cTnI phosphorylation in a time- and dose-dependent manner in neonatal rat cardiomyocytes. These increases were blocked by the antagonist of β1-adrenoceptors. Also, the action of dobutamine was related to the increase of calcium ions and diminished by chelating intracellular calcium. Additionally, dobutamine-induced action was reduced by the inhibition of downstream messengers involved in this calcium-related pathway. Moreover, deletion of PPARδ using siRNA generated the reduction of cTnI phosphorylation in cardiomyocytes treated with dobutamine. Thus, we concluded that PPARδ is increased by dobutamine in cardiac cells.
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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.