Evidence map›Paper›PMID 23564188›Full record

ArticleMolecular and cellular biochemistry2013

LPS induces cardiomyocyte injury through calcium-sensing receptor.

Hong-yu Wang, Xue-yan Liu, Gan Han, Zhu-ying Wang, Xiao-xie Li, Zhi-mei Jiang, Chun-ming Jiang

Open access · hybridAbstract read
In one paragraph

Article in Molecular and cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
1.8field-weighted citation impact, top 13% 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, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. The calcium-sensing receptor in sepsis and septic shock, mechanistic pathways and translational perspectives: a systematic review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Pooled it
  2. Review
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  9. Combination therapy of insulin-like growth factor I and BTP-2 markedly improves lipopolysaccharide-induced liver injury in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  10. Review
  11. Review
  12. The Novel Role of Metabolism-Associated Molecular Patterns in Sepsis.Frontiers in cellular and infection microbiology · 2022
    Review
  13. Review
  14. Article
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  19. Review
  20. Relationship between CaSRs and LPS-injured cardiomyocytes.International journal of clinical and experimental pathology · 2018
    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

7 authors at 3 institutions in 1 country.

Hong-yu WangDepartment of Neonatology, The First Clinical Hospital of Harbin Medical University, Harbin, China.
Xue-yan Liu
Gan Han
Zhu-ying Wang
Xiao-xie Li
Zhi-mei Jiang
Chun-ming Jiang
Harbin Medical University · CNJiamusi University · CNFirst Affiliated Hospital of Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Calcium-sensing receptor (CaSR) belongs to the family C of G-protein coupled receptors. We have previously demonstrated that CaSR could induce apoptosis of cultured neonatal rat ventricular cardiomyocytes in simulated ischemia/reperfusion. It remains unknown whether the CaSR has function in lipopolysaccharide (LPS)-induced myocardial injure. The aim of this study was to investigate whether the CaSR plays a role in LPS-induced myocardial injury. Cultured neonatal rat cardiomyocytes were treated with LPS, with or without pretreatment with the CaSR-specific agonist gadolinium chloride (GdCl3) or the CaSR-specific antagonist NPS2390. Release of TNF-α and IL-6 from cardiomyocytes was observed. Levels of malonaldehyde (MDA), lactate dehydrogenase (LDH), and activity of superoxide dismutase (SOD) were measured. In addition, apoptosis of the cardiomyocytes, [Ca(2+)]i and level of CaSR expression were determined. The results showed that LPS increased cardiomyocytes apoptosis, [Ca(2+)]i, MDA, LDH, TNF-α, IL-6 release, and CaSR protein expression. Compared with LPS treatment alone, pretreatment with GdCl3 further increased apoptosis of cardiomyocytes, MDA, LDH, TNF-α, IL-6 release, [Ca(2+)]i, and the expression of the CaSR protein. Conversely, pretreatment with NPS2390 decreased apoptosis of cardiomyocytes, MDA, LDH, TNF-α, IL-6 release, [Ca(2+)]i and the expression of the CaSR protein. These results demonstrate that LPS could induce cardiomyocyte injury. Moreover, LPS-induced cardiomyocyte injury was related to CaSR-mediated cardiomyocytes apoptosis, TNF-α, IL-6 release, and increase of intracellular calcium.

Indexed as

AdamantaneAnimalsApoptosisCalcium SignalingCells, CulturedGadoliniumInterleukin-6LipopolysaccharidesL-Lactate DehydrogenaseMalondialdehydeMyocytes, CardiacQuinoxalinesRatsRats, Sprague-DawleyReceptors, Calcium-SensingSuperoxide Dismutase2-quinoxaline-carboxamide-N-adamantan-1-ylAdamantaneGadoliniumgadolinium chlorideInterleukin-6LipopolysaccharidesL-Lactate DehydrogenaseMalondialdehydeQuinoxalinesReceptors, Calcium-SensingSuperoxide DismutaseTumor Necrosis Factor-alpha

Identifiers

PMID23564188
PMCPMC3666124
OpenAlexW2067866614

What OpenQuestion holds

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LicenceCC BY
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.