Evidence map›Paper›PMID 35332189›Full record

ArticleScientific reports2022

Oxidative stress facilitates exogenous mitochondria internalization and survival in retinal ganglion precursor-like cells.

Michal Aharoni-Simon, Keren Ben-Yaakov, Maya Sharvit-Bader, Daniel Raz, Yasmin Haim, Waleed Ghannam, Noga Porat, Hana Leiba, Arie Marcovich, Avital Eisenberg-Lerner and 1 more

Abstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
–field-weighted citation impact
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

12 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Mitochondria Transplantation Promotes Corneal Epithelial Wound Healing.Investigative ophthalmology & visual science · 2024
    Article
  10. Article
  11. Review
  12. 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

11 authors.

Michal Aharoni-Simon *Ophthalmology Research Laboratory, Kaplan Medical Center, 76100, Rehovot, Israel. michal.simon@mail.huji.ac.il.
Keren Ben-Yaakov *Ophthalmology Research Laboratory, Kaplan Medical Center, 76100, Rehovot, Israel.
Maya Sharvit-BaderOphthalmology Research Laboratory, Kaplan Medical Center, 76100, Rehovot, Israel.
Daniel RazOphthalmology Research Laboratory, Kaplan Medical Center, 76100, Rehovot, Israel.
Yasmin HaimOphthalmology Research Laboratory, Kaplan Medical Center, 76100, Rehovot, Israel.
Waleed GhannamOphthalmology Research Laboratory, Kaplan Medical Center, 76100, Rehovot, Israel.
Noga PoratOphthalmology Research Laboratory, Kaplan Medical Center, 76100, Rehovot, Israel.
Hana LeibaOphthalmology Research Laboratory, Kaplan Medical Center, 76100, Rehovot, Israel.
Arie MarcovichOphthalmology Research Laboratory, Kaplan Medical Center, 76100, Rehovot, Israel.
Avital Eisenberg-LernerOphthalmology Research Laboratory, Kaplan Medical Center, 76100, Rehovot, Israel.
Ziv RotfogelOphthalmology Research Laboratory, Kaplan Medical Center, 76100, Rehovot, Israel. rotfogel@gmail.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ocular cells are highly dependent on mitochondrial function due to their high demand of energy supply and their constant exposure to oxidative stress. Indeed, mitochondrial dysfunction is highly implicated in various acute, chronic, and genetic disorders of the visual system. It has recently been shown that mitochondrial transplantation (MitoPlant) temporarily protects retinal ganglion cells (RGCs) from cell death during ocular ischemia. Here, we characterized MitoPlant dynamics in retinal ganglion precursor-like cells, in steady state and under oxidative stress. We developed a new method for detection of transplanted mitochondria using qPCR, based on a difference in the mtDNA sequence of C57BL/6 and BALB/c mouse strains. Using this approach, we show internalization of exogenous mitochondria already three hours after transplantation, and a decline in mitochondrial content after twenty four hours. Interestingly, exposure of target cells to moderate oxidative stress prior to MitoPlant dramatically enhanced mitochondrial uptake and extended the survival of mitochondria in recipient cells by more than three fold. Understanding the factors that regulate the exogenous mitochondrial uptake and their survival may promote the application of MitoPlant for treatment of chronic and genetic mitochondrial diseases.

Indexed as

Mitochondrial DiseasesRetinal Ganglion CellsAnimalsMiceMice, Inbred C57BLMitochondriaOxidative Stress

Identifiers

PMID35332189
PMCPMC8948238

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Registered trials

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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.