Evidence map›Paper›PMID 17234167›Full record

ArticleCardiovascular research2007

Impaired perfusion after myocardial infarction is due to reperfusion-induced deltaPKC-mediated myocardial damage.

Fumiaki Ikeno, Koichi Inagaki, Mehrdad Rezaee, Daria Mochly-Rosen

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

23 citing papers in PubMed, 48 citations in OpenAlex.

  1. Trial
  2. Mitochondrial Kinase Signaling for Cardioprotection.International journal of molecular sciences · 2024
    Review
  3. Article
  4. Review
  5. PKCδ causes sepsis-induced cardiomyopathy by inducing mitochondrial dysfunction.American journal of physiology. Heart and circulatory physiology · 2020
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Protein kinase C delta modulates endothelial nitric oxide synthase after cardiac arrest.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2014
    Article
  12. Article
  13. Protein kinase C, an elusive therapeutic target?Nature reviews. Drug discovery · 2012
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Fumiaki IkenoDivision of Cardiovascular Medicine, Stanford University School of Medicine, Stanford, CA 94305-5174, United States.
Koichi Inagaki
Mehrdad Rezaee
Daria Mochly-Rosen
Stanford University · US

Funding

Protein Kinase C Isozymes in Ischemic HeartR01HL052141 · NHLBI · STANFORD UNIVERSITY · PI MOCHLY-ROSEN, DARIA · 1996 to 2021
$8.5M
NHLBI NIH HHS HL52141NHLBI NIH HHS R01 HL052141
6 · The paper itself

Abstract

objectiveTo improve myocardial flow during reperfusion after acute myocardial infarction and to elucidate the molecular and cellular basis that impedes it. According to the AHA/ACC recommendation, an ideal reperfusion treatment in patients with acute myocardial infarction (AMI) should not only focus on restoring flow in the occluded artery, but should aim to reduce microvascular damage to improve blood flow in the infarcted myocardium.

methodsTransgenic mouse hearts expressing the deltaPKC (protein kinase C) inhibitor, deltaV1-1, in their myocytes only were treated with or without the deltaPKC inhibitor after ischemia in an ex vivo AMI model. deltaV1-1 or vehicle was also delivered at reperfusion in an in vivo porcine model of AMI. Microvascular dysfunction was assessed by physiological and histological measurements.

resultsdeltaPKC inhibition in the endothelial cells improved myocardial perfusion in the transgenic mice. In the porcine in vivo AMI model, coronary flow reserve (CFR), which is impaired for 6 days following infarction, was improved immediately following a one-minute treatment at the end of the ischemic period with the deltaPKC-selective inhibitor, deltaV1-1 ( approximately 250 ng/kg), and was completely corrected by 24 h. Myocardial contrast echocardiography, electron microscopy studies, and TUNEL staining demonstrated deltaPKC-mediated microvascular damage. epsilonPKC-induced preconditioning, which also reduces infarct size by >60%, did not improve microvascular function.

conclusionsThese data suggest that deltaPKC activation in the microvasculature impairs blood flow in the infarcted tissue after restoring flow in the occluded artery and that AMI patients with no-reflow may therefore benefit from treatment with a deltaPKC inhibitor given in conjunction with removal of the coronary occlusion.

Indexed as

AnimalsApoptosisCoronary CirculationEnzyme ActivationHumansImmunohistochemistryIn Situ Nick-End LabelingMiceMice, TransgenicModels, AnimalMyocardial InfarctionMyocardial Reperfusion InjuryMyocardiumOligopeptidesProtein Kinase C-deltaSwineOligopeptidesProtein Kinase C-deltaSer-Phe-Asn-Ser-Tyr-Glu-Leu-Gly-Glu-Ser-Leu

Identifiers

PMID17234167
PMCPMC2180159
OpenAlexW1999096158

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.