ArticleExpert review of clinical pharmacology
Clinical pharmacology of cardiac cyclic AMP in human heart failure: too much or too little?
Article in Expert review of clinical pharmacology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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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.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Development of a Nanoscale Protein-Protein Mapping of PDE4 Interface-Disrupting Peptides.Nano letters · 2026Article
- Myocardial metabolic remodeling in human end-stage ischemic and non-ischemic cardiomyopathy.Journal of molecular and cellular cardiology · 2026Article
- Effect of bucladesine calcium combined with metoprolol on heart rate variability and cardiac function prognosis in heart failure patients with chronic arrhythmias.Frontiers in cardiovascular medicine · 2026Article
- An unusual presentation of pheochromocytoma accompanied by catecholamine-induced cardiomyopathy.ESC heart failure · 2025Article
- The dual GLP-1 and GIP receptor agonist tirzapetide provides an unintended interaction with the β-adrenoceptors and plays a role in glucose metabolism in hyperglycemic or senescent cardiac cells.Cardiovascular diabetology · 2025Article
- Cyclic adenosine monophosphate critically modulates cardiac GLP-1 receptor's anti-inflammatory effects.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Cyclic Adenosine Monophosphate in Cardiac and Sympathoadrenal GLP-1 Receptor Signaling: Focus on Anti-Inflammatory Effects.Pharmaceutics · 2024Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
introductionCyclic 3', 5'-adenosine monophosphate (cAMP) is a major signaling hub in cardiac physiology. Although cAMP signaling has been extensively studied in cardiac cells and animal models of heart failure (HF), not much is known about its actual amount present inside human failing or non-failing cardiomyocytes. Since many drugs used in HF work via cAMP, it is crucial to determine the status of its intracellular levels in failing vs. normal human hearts. AREAS COVERED: Only studies performed on explanted/excised cardiac tissues from patients were examined. Studies that contained no data from human hearts or no data on cAMP levels per se were excluded from this perspective's analysis. EXPERT OPINION: Currently, there is no consensus on the status of cAMP levels in human failing vs. non-failing hearts. Several studies on animal models may suggest maladaptive (e.g. pro-apoptotic) effects of cAMP on HF, advocating for cAMP lowering for therapy, but human studies almost universally indicate that myocardial cAMP levels are deficient in human failing hearts. It is the expert opinion of this perspective that intracellular cAMP levels are too low in human failing hearts, contributing to the disease. Strategies to increase (restore), not decrease, these levels should be pursued in human HF.
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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 Socratic graph.