Evidence map›Paper›PMID 19168855›Full record

ReviewCardiovascular research2009

Protein kinase C in heart failure: a therapeutic target?

Suresh Selvaraj Palaniyandi, Lihan Sun, Julio Cesar Batista Ferreira, Daria Mochly-Rosen

Open access · hybridAbstract readReview
In one paragraph

Review in Cardiovascular research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.

0numbers the graph read from it
0cells of the map it votes in
89citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

89 citing papers in PubMed, 191 citations in OpenAlex.

  1. Precision modification of heart failure signaling by CRISPR-Cas9 base editing.Journal of molecular and cellular cardiology · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Identification of Myeloid Protein Kinase C Epsilon as a Novel Atheroprotective Gene.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Article
  6. Article
  7. Review
  8. Article
  9. 12-Cells · 2022
    Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Angiotensin Receptor-Neprilysin Inhibitor (ARNI) and Cardiac Arrhythmias.International journal of molecular sciences · 2021
    Review
  20. Article

29 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 2 countries.

Suresh Selvaraj PalaniyandiDepartment of Chemical and Systems Biology, Stanford University School of Medicine, CCSR, Rm 3145A, 269 Campus Drive, Stanford, CA 94305-5174, USA.
Lihan Sun
Julio Cesar Batista Ferreira
Daria Mochly-Rosen
Stanford University · US

Funding

Hypertrophy, Heart Failure and PKCR01HL076675 · NHLBI · STANFORD UNIVERSITY · PI MOCHLY-ROSEN, DARIA · 2004 to 2008
$1.9M
NHLBI NIH HHS HL76675
6 · The paper itself

Abstract

Heart failure (HF) afflicts about 5 million people and causes 300,000 deaths a year in the United States alone. An integral part of the pathogenesis of HF is cardiac remodelling, and the signalling events that regulate it are a subject of intense research. Cardiac remodelling is the sum of responses of the heart to causes of HF, such as ischaemia, myocardial infarction, volume and pressure overload, infection, inflammation, and mechanical injury. These responses, including cardiomyocyte hypertrophy, myocardial fibrosis, and inflammation, involve numerous cellular and structural changes and ultimately result in a progressive decline in cardiac performance. Pharmacological and genetic manipulation of cultured heart cells and animal models of HF and the analysis of cardiac samples from patients with HF are all used to identify the molecular and cellular mechanisms leading to the disease. Protein kinase C (PKC) isozymes, a family of serine-threonine protein kinase enzymes, were found to regulate a number of cardiac responses, including those associated with HF. In this review, we describe the PKC isozymes that play critical roles in specific aspects of cardiac remodelling and dysfunction in HF.

Indexed as

AnimalsCells, CulturedDisease Models, AnimalFibrosisHeart FailureHumansHypertrophyInflammationIsoenzymesMiceMyocytes, CardiacProtein Kinase CRatsIsoenzymesProtein Kinase C

Identifiers

PMID19168855
PMCPMC2675930
OpenAlexW2004198698

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.