Evidence map›Paper›PMID 31464774›Full record

ReviewJournal of cardiovascular pharmacology2020

cGMP Signaling and Modulation in Heart Failure.

Robert M Blanton

Open access · greenAbstract readReview
In one paragraph

Review in Journal of cardiovascular pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

38 citing papers in PubMed, 58 citations in OpenAlex.

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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 2 countries.

Robert M BlantonMolecular Cardiology Research Institute, Tufts Medical Center, Boston, MA; and.
Institute of Molecular and Cell Biology · RU

Funding

Novel Protein Kinase GI Substrates in Cardiac Remodeling and Blood Pressure ControlR01HL131831 · NHLBI · TUFTS MEDICAL CENTER · PI BLANTON, ROBERT MORRIS · 2016 to 2020
$2.1M
NHLBI NIH HHS R01 HL131831
6 · The paper itself

Abstract

Cyclic GMP (cGMP) represents a classic intracellular second messenger molecule. Over the past 2 decades, important discoveries have identified that cGMP signaling becomes deranged in heart failure (HF) and that cGMP and its main kinase effector, protein kinase G, generally oppose the biological abnormalities contributing to HF, in experimental studies. These findings have influenced the design of clinical trials of cGMP-augmenting drugs in HF patients. At present, the trial results of cGMP-augmenting therapies in HF remain mixed. As detailed in this review, strong evidence now exists that protein kinase G opposes pathologic cardiac remodeling through regulation of diverse biological processes and myocardial substrates. Potential reasons for the failures of cGMP-augmenting drugs in HF may be related to biological mechanisms opposing cGMP or because of certain features of clinical trials, all of which are discussed.

Indexed as

Second Messenger SystemsAnimalsCardiovascular AgentsCyclic GMPCyclic GMP-Dependent Protein KinasesGuanylate CyclaseHeart FailureHumansMolecular Targeted TherapyMyocardiumNitric OxidePhosphoric Diester HydrolasesCardiovascular AgentsCyclic GMPCyclic GMP-Dependent Protein KinasesGuanylate CyclaseNitric OxidePhosphoric Diester Hydrolases

Identifiers

PMID31464774
PMCPMC7044023
OpenAlexW2970837760

What OpenQuestion holds

Textmetadata
LicenceTDM
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.