Evidence map›Paper›PMID 12875985›Full record

ArticleThe American journal of pathology2003

Apoptosis-resistance of hypoxic cells: multiple factors involved and a role for IAP-2.

Zheng Dong, Jin Zhao Wang, Fushin Yu, Manjeri A Venkatachalam

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

41 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
  2. Phosphorescence-basediScience · 2025
    Article
  3. Article
  4. Ruthenium-Based Photoactivated Chemotherapy.Journal of the American Chemical Society · 2023
    Review
  5. Review
  6. Review
  7. Article
  8. Hypoxia Enhances HIF1Stem cells international · 2022
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. VHL-deficient renal cancer cells gain resistance to mitochondria-activating apoptosis inducers by activating AKT through the IGF1R-PI3K pathway.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016
    Article
  16. Article
  17. Review
  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

4 authors at 2 institutions in 1 country.

Zheng DongDepartment of Cellular Biology and Anatomy, Medical College of Georgia, Augusta, Georgia 30912, USA. zdong@mail.mcg.edu
Jin Zhao Wang
Fushin Yu
Manjeri A Venkatachalam
Augusta University · USThe University of Texas Health Science Center at San Antonio · US

Funding

DNA methylation in kidney repair after ischemic AKIR01DK058831 · NIDDK · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI DONG, ZHENG · 2001 to 2025
$7.5M
NIDDK NIH HHS DK58831NIDDK NIH HHS R01 DK058831
6 · The paper itself

Abstract

Hypoxia is an important pathogenic factor in ischemic disease and tumorigenesis. Under hypoxia, some cells are irreversibly damaged, whereas others adapt to the stress and may become more resistant to injury. The mechanism underlying such adaptive responses is unclear. Our recent study showed hypoxic induction of inhibitor of apoptosis protein-2 (IAP-2). Here we have investigated the critical steps in the apoptotic cascade that are affected by hypoxia and have identified a role for IAP-2 in apoptosis resistance of hypoxic cells. The results show that cells cultured in hypoxia became resistant to staurosporine-induced apoptosis. Apoptosis resistance of these cells took place at the mitochondria and in the cytosol. At the mitochondrial level, membrane accumulation of the proapoptotic molecule Bax was suppressed. This was accompanied by less cytochrome c (cyt. c) release from the organelles. In the cytosol, hypoxia induced IAP-2; the cytosol with IAP-2 was resistant to cyt. c-stimulated caspase activation. Of significance, immunodepletion of IAP-2 from the hypoxic cytosol restored its competence for caspase activation. Thus, death resistance of hypoxic cells involves multiple factors targeting different stages of apoptosis, with IAP-2 suppressing caspases in the cytosol.

Indexed as

ApoptosisProto-Oncogene Proteins c-bcl-2Adenosine TriphosphateAnimalsbcl-2-Associated X ProteinCaspasesCell FractionationCell HypoxiaCell LineCysteine Proteinase InhibitorsCytochrome c GroupCytoplasmEnzyme ActivationGlucoseInhibitor of Apoptosis ProteinsKidney TubulesAdenosine TriphosphateBax protein, ratbcl-2-Associated X ProteinCaspasesCysteine Proteinase InhibitorsCytochrome c GroupGlucoseinhibitor of apoptosis, NucleopolyhedrovirusInhibitor of Apoptosis ProteinsProto-Oncogene ProteinsProto-Oncogene Proteins c-bcl-2StaurosporineViral Proteins

Identifiers

PMID12875985
PMCPMC1868200
OpenAlexW1509592700

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.