Evidence map›Paper›PMID 23744887›Full record

ArticleJournal of the American Society of Nephrology : JASN2013

Ouabain protects against Shiga toxin-triggered apoptosis by reversing the imbalance between Bax and Bcl-xL.

Ievgeniia Burlaka, Xiao Li Liu, Johan Rebetz, Ida Arvidsson, Liping Yang, Hjalmar Brismar, Diana Karpman, Anita Aperia

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

25 citing papers in PubMed, 48 citations in OpenAlex.

  1. Cellular signaling pathway of Shiga toxin-induced ATP release.Frontiers in cellular and infection microbiology · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Toxins · 2021
    Review
  10. NaMolecules (Basel, Switzerland) · 2021
    Review
  11. Review
  12. Article
  13. Ouabain-regulated phosphoproteome reveals molecular mechanisms for NaFASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  14. Prompt apoptotic response to high glucose in SGLT-expressing renal cells.American journal of physiology. Renal physiology · 2019
    Article
  15. Article
  16. Review
  17. Article
  18. Alpha 2 NaScientific reports · 2017
    Article
  19. Src-independent ERK signaling through the rat α3 isoform of Na/K-ATPase.American journal of physiology. Cell physiology · 2017
    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 2 countries.

Ievgeniia BurlakaDepartment of Women's and Children's Health, Karolinska Institutet, Astrid Lindgren Children's Hospital, Research Lab, Stockholm, Sweden.
Xiao Li Liu
Johan Rebetz
Ida Arvidsson
Liping Yang
Hjalmar Brismar
Diana Karpman
Anita Aperia
Lund University · SEKTH Royal Institute of Technology · SENantong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hemolytic uremic syndrome, a life-threatening disease often accompanied by acute renal failure, usually occurs after gastrointestinal infection with Shiga toxin 2 (Stx2)-producing Escherichia coli. Stx2 binds to the glycosphingolipid globotriaosylceramide receptor, expressed by renal epithelial cells, and triggers apoptosis by activating the apoptotic factor Bax. Signaling via the ouabain/Na,K-ATPase/IP3R/NF-κB pathway increases expression of Bcl-xL, an inhibitor of Bax, suggesting that ouabain might protect renal cells from Stx2-triggered apoptosis. Here, exposing rat proximal tubular cells to Stx2 in vitro resulted in massive apoptosis, upregulation of the apoptotic factor Bax, increased cleaved caspase-3, and downregulation of the survival factor Bcl-xL; co-incubation with ouabain prevented all of these effects. Ouabain activated the NF-κB antiapoptotic subunit p65, and the inhibition of p65 DNA binding abolished the antiapoptotic effect of ouabain in Stx2-exposed tubular cells. Furthermore, in vivo, administration of ouabain reversed the imbalance between Bax and Bcl-xL in Stx2-treated mice. Taken together, these results suggest that ouabain can protect the kidney from the apoptotic effects of Stx2.

Indexed as

AnimalsApoptosisbcl-2-Associated X Proteinbcl-X ProteinCaspase 3Caspase 8Cells, CulturedDisease Models, AnimalDose-Response Relationship, DrugEnzyme InhibitorsInositol 1,4,5-Trisphosphate ReceptorsIn Vitro TechniquesKidney Tubules, ProximalMaleMiceMice, Inbred C57BLbcl-2-Associated X Proteinbcl-X ProteinCaspase 3Caspase 8Enzyme InhibitorsInositol 1,4,5-Trisphosphate ReceptorsNF-kappa BOuabainShiga Toxin 2Sodium-Potassium-Exchanging ATPase

Identifiers

PMID23744887
PMCPMC3752948
OpenAlexW2113033827

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.