Evidence map›Paper›PMID 19717737›Full record

ReviewAmerican journal of physiology. Heart and circulatory physiology2009

JAK redux: a second look at the regulation and role of JAKs in the heart.

Mazen Kurdi, George W Booz

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

34 citing papers in PubMed, 76 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. The Role of Genetics in Peripartum Cardiomyopathy.Journal of cardiovascular translational research · 2017
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Inhibition of Janus kinase signaling during controlled mechanical ventilation prevents ventilation-induced diaphragm dysfunction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014
    Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Functions of cyclophilin A in atherosclerosis.Experimental and clinical cardiology · 2013
    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

2 authors at 2 institutions in 2 countries.

Mazen KurdiDepartment of Chemistry and Biochemistry, Faculty of Sciences, Lebanese University, Rafic Hariri Educational Campus, Hadath, Lebanon.
George W Booz
Lebanese University · LBUniversity of Mississippi Medical Center · US

Funding

Regulation of IL-6-Type Cytokine Cardioprotective Signaling in the Ischemic HeartR01HL088101 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI BOOZ, GEORGE W. · 2008 to 2012
$2.0M
NHLBI NIH HHS 1-R01-HL-088101
6 · The paper itself

Abstract

A number of type 1 receptor cytokine family members protect the heart from acute and chronic oxidative stress. This protection involves activation of two intracellular signaling cascades: the reperfusion injury salvage kinase (RISK) pathway, which entails activation of phosphatidylinositol 3-kinase (PI3-kinase) and ERK1/2, and JAK-STAT signaling, which involves activation of transcription factor signal transducer and activator of transcription 3 (STAT3). Obligatory for activation of both RISK and STAT3 by nearly all of these cytokines are the kinases JAK1 and JAK2. Yet surprisingly little is known about how JAK1 and JAK2 are regulated in the heart or how they couple to PI3-kinase activation. Although the JAKs are linked to antioxidative stress programs in the heart, we recently reported that these kinases are inhibited by oxidative stress in cardiac myocytes. In contrast, others have reported that cardiac JAK2 is activated by acute oxidative stress by an undefined process. Here we summarize recent insights into the regulation of JAK1 and JAK2. Besides oxidative stress, inhibitory regulation involves phosphorylation, nitration, and intramolecular restraints. Stimulatory regulation involves phosphorylation and adaptor proteins. The net effect of stress on JAK activity in the heart likely represents the sum of both inhibitory and stimulatory processes, along with their dynamic interaction. Thus the regulation of JAKs in the heart, once touted as the paragon of simplicity, is proving rather complicated indeed, requiring a second look. It is our contention that a better understanding of the regulation of this kinase family that is implicated in cardiac protection could translate into effective therapeutic strategies for preventing myocardial damage or repairing the injured heart.

Indexed as

Oxidative StressSignal TransductionAmino Acid SequenceAnimalsCytokinesEnzyme ActivationHeart DiseasesHumansJanus Kinase 1Janus Kinase 2Molecular Sequence DataMyocardiumOxidation-ReductionPhosphatidylinositol 3-KinasesPhosphorylationProto-Oncogene Proteins c-aktCytokinesJanus Kinase 1Janus Kinase 2Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSTAT3 Transcription Factor

Identifiers

PMID19717737
PMCPMC2781365
OpenAlexW2122401488

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.