Evidence map›Paper›PMID 18728217›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2008

Ischemic preconditioning-induced cardioprotection is lost in mice with immunoproteasome subunit low molecular mass polypeptide-2 deficiency.

Zheqing P Cai, Zhenyun Shen, Luc Van Kaer, Lewis C Becker

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

39 citing papers in PubMed, 63 citations in OpenAlex.

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  17. Altered ubiquitin-proteasome signaling in right ventricular hypertrophy and failure.American journal of physiology. Heart and circulatory physiology · 2013
    Article
  18. Article
  19. The ubiquitin proteasome system and myocardial ischemia.American journal of physiology. Heart and circulatory physiology · 2013
    Review
  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

4 authors at 4 institutions in 2 countries.

Zheqing P CaiDivision of Cardiology, Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland, USA. czheqin1@jhmi.edu
Zhenyun Shen
Luc Van Kaer
Lewis C Becker
Johns Hopkins Medicine · USJohns Hopkins University · USPeking University · CNVanderbilt University · US

Funding

Stat3 in Post-Ischemic Myocardial InflammationP01HL065608 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI BECKER, LEWIS C · 2000 to 2011
$22.0M
NHLBI NIH HHS P01 HL065608NHLBI NIH HHS P01-HL65608
6 · The paper itself

Abstract

The ubiquitin-proteasome system plays an important role in many cellular processes through degradation of specific proteins. Low molecular mass polypeptide 2 (LMP-2 or beta(1i)) is one important subunit of the immunoproteasome. Ischemic preconditioning (IPC) activates cell signaling pathways and generates cardioprotection but has not been linked to LMP-2 function previously. LMP-2 knockout mice (C57BL6 background) and wild-type C57BL6 mice were subjected to 30 min of ischemia (I-30) and 120 min of reperfusion (R-120) with or without preceding IPC (10 min of infusion and 5 min of reperfusion). IPC significantly increased left ventricular developed pressure and decreased infarct size in wild-type mice, but this protective effect of IPC was lost in LMP-2 knockout mice. IPC-mediated degradation of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) and activation of the downstream protein kinase Akt were impaired in LMP-2 knockout hearts. The impairment of PTEN degradation was associated with defective immunoproteasomes and decreased proteolytic activities. When LMP-2 knockout mice were pretreated with the PTEN inhibitor bpV(HOpic), cardiac function was significantly improved, and myocardial infarct size was significantly reduced after I-30/R-120. In conclusion, LMP-2 is required for normal proteasomal function and IPC induction in the heart. Its action may be related to PTEN protein degradation.

Indexed as

Ischemic Preconditioning, MyocardialAnimalsCysteine EndopeptidasesDown-RegulationHeartMaleMiceMice, KnockoutMyocardial InfarctionProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseCysteine EndopeptidasesLMP-2 proteinProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePten protein, mouse

Identifiers

PMID18728217
PMCPMC2614607
OpenAlexW2000091638

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.