Evidence map›Paper›PMID 20937286›Full record

ReviewJournal of molecular and cellular cardiology2011

Protein kinase Cα as a heart failure therapeutic target.

Qinghang Liu, Jeffery D Molkentin

Open access · greenAbstract readReview
In one paragraph

Review in Journal of molecular and cellular cardiology, 2011. 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
2.0field-weighted citation impact, top 14% 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, 75 citations in OpenAlex.

  1. Trial
  2. Precision modification of heart failure signaling by CRISPR-Cas9 base editing.Journal of molecular and cellular cardiology · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Cardioprotective Strategies After Ischemia-Reperfusion Injury.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2024
    Review
  7. Review
  8. Article
  9. Calcium-Signalling in Human Glaucoma Lamina Cribrosa Myofibroblasts.International journal of molecular sciences · 2023
    Review
  10. Putative role of natural products as Protein Kinase C modulator in different disease conditions.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2021
    Review
  11. Article
  12. Upregulation of COX-2 and PGEJournal of inflammation research · 2021
    Article
  13. Article
  14. Article
  15. Protein Kinase C: Targets to Regenerate Brain Injuries?Frontiers in cell and developmental biology · 2019
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Frontiers in cardiovascular medicine · 2018
    Article
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

2 authors at 1 institution in 1 country.

Qinghang LiuDepartment of Pediatrics, Division of Molecular Cardiovascular Biology, University of Cincinnati, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Jeffery D Molkentin
Cincinnati Children's Hospital Medical Center · US

Funding

Thrombospondin 4 regulates adaptive ER stress responseRenewal - Resubmission - 1R01HL105924 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI Jeffery D Molkentin · 2011 to 2026
$7.3M
CARDIAC HYPERTROPHIC INTRACELLULAR SIGNALING PATHWAYSR01HL062927 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI ROBBINS, JEFFREY · 1999 to 2013
$3.9M
Molecular Pathways Controlling Cardiac Gene ExpressionR37HL060562 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI MOLKENTIN, JEFFERY D · 2008 to 2017
$3.8M
Howard Hughes Medical InstituteNHLBI NIH HHS R01 HL062927NHLBI NIH HHS R01 HL105924NHLBI NIH HHS R37 HL060562
6 · The paper itself

Abstract

Heart failure afflicts ~5 million people and causes ~300,000 deaths a year in the United States alone. Heart failure is defined as a deficiency in the ability of the heart to pump sufficient blood in response to systemic demands, which results in fatigue, dyspnea, and/or edema. Identifying new therapeutic targets is a major focus of current research in the field. We and others have identified critical roles for protein kinase C (PKC) family members in programming aspects of heart failure pathogenesis. More specifically, mechanistic data have emerged over the past 6-7 years that directly implicate PKCα, a conventional PKC family member, as a nodal regulator of heart failure propensity. Indeed, deletion of the PKCα gene in mice, or its inhibition in rodents with drugs or a dominant negative mutant and/or inhibitory peptide, has shown dramatic protective effects that antagonize the development of heart failure. This review will weigh all the evidence implicating PKCα as a novel therapeutic target to consider for the treatment of heart failure. This article is part of a special issue entitled "Key Signaling Molecules in Hypertrophy and Heart Failure."

Indexed as

Molecular Targeted TherapyAnimalsDrug Evaluation, PreclinicalGene ExpressionHeart FailureHumansMiceMice, KnockoutMyocardial ContractionMyocardiumProtein Kinase C-alphaProtein Kinase InhibitorsProtein Kinase C-alphaProtein Kinase Inhibitors

Identifiers

PMID20937286
PMCPMC3204459
OpenAlexW1997079073

What Socratic 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 Socratic graph.