Evidence map›Paper›PMID 30583467›Full record

ReviewInternational journal of molecular sciences2018

A Dual Role of Heme Oxygenase-1 in Cancer Cells.

Shih-Kai Chiang, Shuen-Ei Chen, Ling-Chu Chang

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 284 papers.

0numbers the graph read from it
0cells of the map it votes in
284citing papers in PubMed
11.9field-weighted citation impact, top 1% 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

284 citing papers in PubMed, 454 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Heme oxygenase-1 in thyroid cancer: a context-dependent regulator.Journal of endocrinological investigation · 2026
    Review
  5. Haemolytic injury and cardiovascular disease.Nature reviews. Cardiology · 2026
    Review
  6. Intracellular Crosstalk of the Gasotransmitter Trio (NO, CO, HInternational journal of molecular sciences · 2026
    Review
  7. Article
  8. Article
  9. Article
  10. Ginsenoside Rh4 Triggers Ferroptosis in Lung Cancer: TargetingInternational journal of molecular sciences · 2026
    Article
  11. Review
  12. ERM Inhibition Confers Ferroptosis Resistance through ROS-Induced NRF2 Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. Review

224 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Shih-Kai ChiangDepartment of Animal Science, National Chung Hsing University, Taichung 40227, Taiwan. shihkaichiang@gmail.com.
Shuen-Ei ChenDepartment of Animal Science, National Chung Hsing University, Taichung 40227, Taiwan. chenshuenei@hotmail.com.
Ling-Chu ChangChinese Medicinal Research and Development Center, China Medical University Hospital, Taichung 40447, Taiwan. t27602@mail.cmuh.org.tw.ORCID 0000-0002-7905-580X
National Chung Hsing University · TWChina Medical University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Heme oxygenase (HO)-1 is known to metabolize heme into biliverdin/bilirubin, carbon monoxide, and ferrous iron, and it has been suggested to demonstrate cytoprotective effects against various stress-related conditions. HO-1 is commonly regarded as a survival molecule, exerting an important role in cancer progression and its inhibition is considered beneficial in a number of cancers. However, increasing studies have shown a dark side of HO-1, in which HO-1 acts as a critical mediator in ferroptosis induction and plays a causative factor for the progression of several diseases. Ferroptosis is a newly identified iron- and lipid peroxidation-dependent cell death. The critical role of HO-1 in heme metabolism makes it an important candidate to mediate protective or detrimental effects via ferroptosis induction. This review summarizes the current understanding on the regulatory mechanisms of HO-1 in ferroptosis. The amount of cellular iron and reactive oxygen species (ROS) is the determinative momentum for the role of HO-1, in which excessive cellular iron and ROS tend to enforce HO-1 from a protective role to a perpetrator. Despite the dark side that is related to cell death, there is a prospective application of HO-1 to mediate ferroptosis for cancer therapy as a chemotherapeutic strategy against tumors.

Indexed as

Cell DeathAnimalsCell Line, TumorDisease Models, AnimalDrug TherapyHemeHeme Oxygenase-1HumansIronLipid PeroxidationNeoplasmsReactive Oxygen SpeciesXenograft Model Antitumor AssaysHemeHeme Oxygenase-1IronReactive Oxygen Specieschemotherapyferroptosisglutathioneheme oxygenase-1ironreactive oxygen species

Identifiers

PMID30583467
PMCPMC6337503
OpenAlexW2905675459

What OpenQuestion holds

Textmetadata
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.