Evidence map›Paper›PMID 17332439›Full record

ReviewCirculation research2007

Regulation of phosphodiesterase 3 and inducible cAMP early repressor in the heart.

Chen Yan, Clint L Miller, Jun-ichi Abe

Open access · bronzeAbstract readReview
In one paragraph

Review in Circulation research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

53 citing papers in PubMed, 109 citations in OpenAlex.

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  20. Roles of PDE1 in Pathological Cardiac Remodeling and Dysfunction.Journal of cardiovascular development and disease · 2018
    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

3 authors at 2 institutions in 1 country.

Chen YanCenter for Cardiovascular Research, Aab Institute of Biomedical Science, University of Rochester School of Medicine and Dentistry, Rochester, NY 14642, USA. Chen_Yan@urmc.rochester.edu
Clint L Miller
Jun-ichi Abe
University of Rochester · USRochester Institute of Technology · US

Funding

Vascular Inflammation and AtherosclerosisP01HL077789 · NHLBI · UNIVERSITY OF ROCHESTER · PI BERK, BRADFORD C · 2005 to 2009
$10.1M
ROLE OF P90RSK IN DIABETIC CARDIOMYOPATHYR01HL066919 · NHLBI · UNIVERSITY OF ROCHESTER · PI ABE, JUN-ICHI · 2000 to 2003
$1.6M
Big MAP Kinase 1-Cx 43 Signaling in Ischemia InjuryR01GM071485 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI YANG, JAY · 2005 to 2008
$1.5M
NHLBI NIH HHS HL-077789NHLBI NIH HHS HL077789NHLBI NIH HHS HL-66919NHLBI NIH HHS P01 HL077789NHLBI NIH HHS R01 HL066919NIGMS NIH HHS GM-071485NIGMS NIH HHS R01 GM071485
6 · The paper itself

Abstract

Growing evidence suggests that multiple spatially, temporally, and functionally distinct pools of cyclic nucleotides exist and regulate cardiac performance, from acute myocardial contractility to chronic gene expression and cardiac structural remodeling. Cyclic nucleotide phosphodiesterases (PDEs), by hydrolyzing cAMP and cyclic GMP, regulate the amplitude, duration, and compartmentation of cyclic nucleotide-mediated signaling. In particular, PDE3 enzymes play a major role in regulating cAMP metabolism in the cardiovascular system. PDE3 inhibitors, by raising cAMP content, have acute inotropic and vasodilatory effects in treating congestive heart failure but have increased mortality in long-term therapy. PDE3A expression is downregulated in human and animal failing hearts. In vitro, inhibition of PDE3A function is associated with myocyte apoptosis through sustained induction of a transcriptional repressor ICER (inducible cAMP early repressor) and thereby inhibition of antiapoptotic molecule Bcl-2 expression. Sustained induction of ICER may also cause the change of other protein expression implicated in human and animal failing hearts. These data suggest that the downregulation of PDE3A observed in failing hearts may play a causative role in the progression of heart failure, in part, by inducing ICER and promoting cardiac myocyte dysfunction. Hence, strategies that maintain PDE3A function may represent an attractive approach to circumvent myocyte apoptosis and cardiac dysfunction.

Indexed as

3',5'-Cyclic-AMP PhosphodiesterasesAnimalsCardiovascular DiseasesCyclic AMP Response Element ModulatorCyclic Nucleotide Phosphodiesterases, Type 3Feedback, PhysiologicalHeartHumansMyocardium3',5'-Cyclic-AMP PhosphodiesterasesCyclic AMP Response Element ModulatorCyclic Nucleotide Phosphodiesterases, Type 3PDE3A protein, human

Identifiers

PMID17332439
PMCPMC4115784
OpenAlexW2130919931

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.