Evidence mapPaperPMID 37403791Full record

ArticleExpert review of clinical pharmacology

Clinical pharmacology of cardiac cyclic AMP in human heart failure: too much or too little?

Anastasios Lymperopoulos

Open access · greenAbstract read
In one paragraph

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.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
2.2field-weighted citation impact, top 11% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. 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.] · 2024
    Article
  7. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Anastasios LymperopoulosLaboratory for the Study of Neurohormonal Control of the Circulation, Department of Pharmaceutical Sciences, Nova Southeastern University Barry and Judy Silverman College of Pharmacy, Fort Lauderdale, FL, USA.
Nova Southeastern University · US

Funding

Trans-omic analysis of epicardial adipose tissue in atrial fibrillationR01HL155718 · NHLBI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI JEFFREY J GOLDBERGER · 2022 to 2024
$2.1M
NHLBI NIH HHS R01 HL155718
6 · The paper itself

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.

Indexed as

Cyclic AMPHeart FailureAnimalsHumansMyocardiumMyocytes, CardiacSignal TransductionCyclic AMPAdenylyl cyclasecardiac functioncyclic AMPG protein-coupled receptorheart failurehuman heartprotein kinase asignal transduction

Identifiers

PMID37403791
PMCPMC10529896
OpenAlexW4383186664

What Socratic holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

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.