ReviewJournal of cardiovascular translational research2010
Targeting cyclic nucleotide phosphodiesterase in the heart: therapeutic implications.
Review in Journal of cardiovascular translational research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 58 citations in OpenAlex.
- Advancing drug development for atrial fibrillation by prioritising findings from human genetic association studies.EBioMedicine · 2024Article
- Article
- Functional characteristics and research trends of PDE11A in human diseases (Review).Molecular medicine reports · 2022Article
- Genome-Wide Association Study Based on Random Regression Model Reveals Candidate Genes Associated with Longitudinal Data in Chinese Simmental Beef Cattle.Animals : an open access journal from MDPI · 2021Article
- Various subtypes of phosphodiesterase inhibitors differentially regulate pulmonary vein and sinoatrial node electrical activities.Experimental and therapeutic medicine · 2020Article
- Cellular Protein Quality Control in Diabetic Cardiomyopathy: From Bench to Bedside.Frontiers in cardiovascular medicine · 2020Review
- Rolipram, a PDE4 Inhibitor, Enhances the Inotropic Effect of Rat Heart by Activating SERCA2a.Frontiers in pharmacology · 2019Article
- cGMP Signaling in the Cardiovascular System-The Role of Compartmentation and Its Live Cell Imaging.International journal of molecular sciences · 2018Review
- Molecular inotropy mediated by cardiac miR-based PDE4D/PRKAR1α/phosphoprotein signaling.Scientific reports · 2016Article
- Interaction between phosphodiesterases in the regulation of the cardiac β-adrenergic pathway.Journal of molecular and cellular cardiology · 2015Article
- Clinical and molecular genetics of the phosphodiesterases (PDEs).Endocrine reviews · 2014Review
- Therapeutic potential of PDE modulation in treating heart disease.Future medicinal chemistry · 2013Review
- Phosphodiesterase type 3A regulates basal myocardial contractility through interacting with sarcoplasmic reticulum calcium ATPase type 2a signaling complexes in mouse heart.Circulation research · 2013Article
- Cardiac cyclic nucleotide phosphodiesterases: function, regulation, and therapeutic prospects.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2012Review
- Biochemical and molecular aspects of vascular adrenergic regulation of blood pressure in the elderly.International journal of hypertension · 2012Article
- Phosphodiesterase function and endocrine cells: links to human disease and roles in tumor development and treatment.Current opinion in pharmacology · 2011Review
- Phosphodiesterase 4D regulates baseline sarcoplasmic reticulum Ca2+ release and cardiac contractility, independently of L-type Ca2+ current.Circulation research · 2011Article
- Compartmentalization of beta-adrenergic signals in cardiomyocytes.Circulation research · 2011Review
- Phosphodiesterases and cardiac cGMP: evolving roles and controversies.Trends in pharmacological sciences · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The second messengers, cAMP and cGMP, regulate a number of physiological processes in the myocardium, from acute contraction/relaxation to chronic gene expression and cardiac structural remodeling. Emerging evidence suggests that multiple spatiotemporally distinct pools of cyclic nucleotides can discriminate specific cellular functions from a given cyclic nucleotide-mediated signal. Cyclic nucleotide phosphodiesterases (PDEs), by hydrolyzing intracellular cyclic AMP and/or cyclic GMP, control the amplitude, duration, and compartmentation of cyclic nucleotide signaling. To date, more than 60 different isoforms have been described and grouped into 11 broad families (PDE1-PDE11) based on differences in their structure, kinetic and regulatory properties, as well as sensitivity to chemical inhibitors. In the heart, PDE isozymes from at least six families have been investigated. Studies using selective PDE inhibitors and/or genetically manipulated animals have demonstrated that individual PDE isozymes play distinct roles in the heart by regulating unique cyclic nucleotide signaling microdomains. Alterations of PDE activity and/or expression have also been observed in various cardiac disease models, which may contribute to disease progression. Several family-selective PDE inhibitors have been used clinically or pre-clinically for the treatment of cardiac or vascular-related diseases. In this review, we will highlight both recent advances and discrepancies relevant to cardiovascular PDE expression, pathophysiological function, and regulation. In particular, we will emphasize how these properties influence current and future development of PDE inhibitors for the treatment of pathological cardiac remodeling and dysfunction.
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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.