Evidence map›Paper›PMID 21909975›Full record

ArticleJournal of molecular medicine (Berlin, Germany)2011

Inhibition of endoplasmic reticulum stress by intermedin(1-53) protects against myocardial injury through a PI3 kinase-Akt signaling pathway.

Xu Teng, Junqiu Song, Gaigai Zhang, Yan Cai, Fang Yuan, Jie Du, Chaoshu Tang, Yongfen Qi

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of molecular medicine (Berlin, Germany), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

26 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. IntermedinAging · 2020
    Article
  11. Article
  12. Article
  13. Review
  14. IntermedinInflammation · 2018
    Article
  15. Article
  16. Article
  17. IntermedinJournal of atherosclerosis and thrombosis · 2016
    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

8 authors at 3 institutions in 1 country.

Xu TengThe Key Laboratory of Remodeling-related Cardiovascular Diseases, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing An Zhen Hospital, Capital Medical University, Ministry of Education, China.
Junqiu Song
Gaigai Zhang
Yan Cai
Fang Yuan
Jie Du
Chaoshu Tang
Yongfen Qi
Capital Medical University · CNPeking University · CNHebei Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intermedin (IMD) is a novel member of the calcitonin/calcitonin gene-related peptide family. We aimed to explore whether the cardioprotective effect of IMD is mediated by inhibiting myocardial endoplasmic reticulum (sarcoplasmic reticulum) stress (ERS). In vitro, IMD(1-53) (10(-9), 10(-8), and 10(-7) mol/l) directly inhibited the upregulation of ERS markers such as glucose-regulated protein 78, CCAAT/enhancer binding protein homologous protein, and caspase-12 induced by the ERS inducers tunicamycin (Tm, 10 mg/ml) or dithiothreitol (DTT, 2 mmol/l) in cardiac tissue. IMD(1-53) also inhibited Tm- or DTT-induced upregulation of cleaved activating transcription factor 6 and 4. These inhibitory effects of IMD(1-53) were abolished by the IMD receptor antagonist IMD(17-47) (10(-6) mol/l) and phosphoinositide 3-kinase inhibitor LY294002 (10 μmol/l). However, preincubation with PD98059 (20 μmol/l), an extracellular signal-regulated protein kinase inhibitor, and H89 (10 μmol/l), a protein kinase A inhibitor, could not block the ERS-inhibiting effects of IMD(1-53). Furthermore, in an in vivo model of myocardium ischemia/reperfusion (I/R) in rats, administration of IMD(1-53) (20 nmol/kg, intravenously) greatly attenuated ERS and ameliorated myocardium impairment induced by I/R. IMD(1-53) could exert its cardioprotective effect by inhibiting myocardial ERS, which might be mediated by the phosphoinositide 3-kinase/Akt signaling pathway.

Indexed as

AnimalsCardiotonic AgentsCaspase 12Disease Models, AnimalEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressHeat-Shock ProteinsHSP70 Heat-Shock ProteinsIn Vitro TechniquesL-Lactate DehydrogenaseMaleMalondialdehydeMembrane ProteinsMyocardial Reperfusion InjuryMyocardiumPeptide HormonesADM2 protein, humanCardiotonic AgentsCaspase 12Ddit3 protein, ratEndoplasmic Reticulum Chaperone BiPglucose-regulated proteinsGRP78 protein, ratHeat-Shock ProteinsHSP70 Heat-Shock ProteinsL-Lactate DehydrogenaseMalondialdehydeMembrane ProteinsPeptide HormonesPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTranscription Factor CHOP

Identifiers

PMID21909975
OpenAlexW2466034850

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.