Evidence map›Paper›PMID 22383703›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2012

Targeted focal adhesion kinase activation in cardiomyocytes protects the heart from ischemia/reperfusion injury.

Zhaokang Cheng, Laura A DiMichele, Zeenat S Hakim, Mauricio Rojas, Christopher P Mack, Joan M Taylor

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

27 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. FAK Family Kinases in Vascular Diseases.International journal of molecular sciences · 2020
    Review
  10. Integrative Analysis of Expression Profiles of MicroRNAs and mRNAs in Treatment of Acute Myocardial Infarction with Compound Longmaining Decoction.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Signaling Pathways in Cardiac Myocyte Apoptosis.BioMed research international · 2016
    Review
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 1 institution in 1 country.

Zhaokang ChengDepartment of Pathology and Laboratory Medicine, University of North Carolina, Chapel Hill, 27599, USA.
Laura A DiMichele
Zeenat S Hakim
Mauricio Rojas
Christopher P Mack
Joan M Taylor
Mahindra and Mahindra Limited (India) · IN

Funding

Genetic and epigenetic regulation of vascular smooth muscle cell phenotype and contractilityR01HL109607 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI MACK, CHRISTOPHER P. · 2012 to 2022
$3.0M
FAK Signaling in cardiac growth and hypertrophyR01HL081844 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI TAYLOR, JOAN M · 2005 to 2013
$2.6M
Adhesion Signaling in Vascular Growth and DevelopmentR01HL071054 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI TAYLOR, JOAN M. · 2003 to 2006
$1.2M
NHLBI NIH HHS HL-071054NHLBI NIH HHS HL-081844NHLBI NIH HHS R01 HL071054NHLBI NIH HHS R01 HL081844NHLBI NIH HHS R01 HL109607
6 · The paper itself

Abstract

objectiveWe previously reported that cardiac-restricted deletion of focal adhesion kinase (FAK) exacerbated myocyte death following ischemia/reperfusion (I/R). Here, we interrogated whether targeted elevation of myocardial FAK activity could protect the heart from I/R injury. METHODS AND

resultsTransgenic mice were generated with myocyte-specific expression of a FAK variant (termed SuperFAK) that conferred elevated allosteric activation. FAK activity in unstressed transgenic hearts was modestly elevated, but this had no discernable effect on anabolic heart growth or cardiac function. Importantly, SuperFAK hearts exhibited a dramatic increase in FAK activity and a reduction in myocyte apoptosis and infarct size 24 to 72 hours following I/R. Moreover, serial echocardiography revealed that the transgenic mice were protected from cardiac decompensation for up to 8 weeks following surgery. Mechanistic studies revealed that elevated FAK activity protected cardiomyocytes from I/R-induced apoptosis by enhancing nuclear factor-κB (NF-κB)-dependent survival signaling during the early period of reperfusion (30 and 60 minutes). Moreover, adenoviral-mediated expression of SuperFAK in cultured cardiomyocytes attenuated H(2)O(2) or hypoxia/reoxygenation-induced apoptosis, whereas blockade of the NF-κB pathway using a pharmacological inhibitor or small interfering RNAs completely abolished the beneficial effect of SuperFAK.

conclusionsEnhancing cardiac FAK activity attenuates I/R-induced myocyte apoptosis through activation of the prosurvival NF-κB pathway and may represent a novel therapeutic strategy for ischemic heart diseases.

Indexed as

Genetic TherapyAnimalsApoptosisCells, CulturedDisease Models, AnimalEnzyme ActivationFocal Adhesion Protein-Tyrosine KinasesHydrogen PeroxideMaleMiceMice, TransgenicMyocardial InfarctionMyocardial Reperfusion InjuryMyocytes, CardiacNF-kappa BRatsFocal Adhesion Protein-Tyrosine KinasesHydrogen PeroxideNF-kappa B

Identifiers

PMID22383703
PMCPMC4237311
OpenAlexW2041318682

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.