Evidence map›Paper›PMID 36611912›Full record

ArticleCells2022

Role of Mitochondrial Iron Overload in Mediating Cell Death in H9c2 Cells.

Eddie Tam, Hye Kyoung Sung, Nhat Hung Lam, Sally You, Sungji Cho, Saher M Ahmed, Ali A Abdul-Sater, Gary Sweeney

Open access · goldAbstract read
In one paragraph

Article in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Iron Dysregulation in Cardiovascular Diseases.Reviews in cardiovascular medicine · 2024
    Review
  12. Article
  13. Review
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 1 institution in 1 country.

Eddie TamDepartment of Biology, York University, Toronto, ON M3J 1P3, Canada.
Hye Kyoung SungDepartment of Biology, York University, Toronto, ON M3J 1P3, Canada.
Nhat Hung LamDepartment of Biology, York University, Toronto, ON M3J 1P3, Canada.
Sally YouDepartment of Biology, York University, Toronto, ON M3J 1P3, Canada.
Sungji ChoDepartment of Biology, York University, Toronto, ON M3J 1P3, Canada.
Saher M AhmedDepartment of Biology, York University, Toronto, ON M3J 1P3, Canada.
Ali A Abdul-SaterMuscle Health Research Centre, School of Kinesiology and Health Science, York University, Toronto, ON M3J 1P3, Canada.
Gary SweeneyDepartment of Biology, York University, Toronto, ON M3J 1P3, Canada.
York University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Iron overload (IO) is associated with cardiovascular diseases, including heart failure. Our study's aim was to examine the mechanism by which IO triggers cell death in H9c2 cells. IO caused accumulation of intracellular and mitochondrial iron as shown by the use of iron-binding fluorescent reporters, FerroOrange and MitoFerroFluor. Expression of cytosolic and mitochondrial isoforms of Ferritin was also induced by IO. IO-induced iron accumulation and cellular ROS was rapid and temporally linked. ROS accumulation was detected in the cytosol and mitochondrial compartments with CellROX, DCF-DA and MitoSOX fluorescent dyes and partly reversed by the general antioxidant N-acetyl cysteine or the mitochondrial antioxidant SkQ1. Antioxidants also reduced the downstream activation of apoptosis and lytic cell death quantified by Caspase 3 cleavage/activation, mitochondrial Cytochrome c release, Annexin V/Propidium iodide staining and LDH release of IO-treated cells. Finally, overexpression of MitoNEET, an outer mitochondrial membrane protein involved in the transfer of Fe-S clusters between mitochondrial and cytosol, was observed to lower iron and ROS accumulation in the mitochondria. These alterations were correlated with reduced IO-induced cell death by apoptosis in MitoNEET-overexpressing cells. In conclusion, IO mediates H9c2 cell death by causing mitochondrial iron accumulation and subsequent general and mitochondrial ROS upregulation.

Indexed as

AntioxidantsIron OverloadCell DeathHumansIronMitochondriaReactive Oxygen SpeciesAntioxidantsIronReactive Oxygen Speciescell deathiron overloadmitochondriaMitoNEETreactive oxygen species

Identifiers

PMID36611912
PMCPMC9818517
OpenAlexW4313414750

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.