Evidence map›Paper›PMID 27627835›Full record

ArticleAutophagy2016

Mitochondrial quality control: Cell-type-dependent responses to pathological mutant mitochondrial DNA.

Adriana Malena, Boris Pantic, Doriana Borgia, Gianluca Sgarbi, Giancarlo Solaini, Ian J Holt, Antonella Spinazzola, Egle Perissinotto, Marco Sandri, Alessandra Baracca and 1 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Autophagy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. Review
  3. The Pro-Oncogenic Protein IFInternational journal of molecular sciences · 2023
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Intracellular quality control of mitochondrial DNA: evidence and limitations.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020
    Review
  10. Article
  11. Article
  12. Sarcopenia: Aging-Related Loss of Muscle Mass and Function.Physiological reviews · 2019 · on this map
    Review
  13. Article
  14. 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.

Adriana Malenaa Department of Neurosciences , University of Padova , Italy.
Boris Pantica Department of Neurosciences , University of Padova , Italy.
Doriana Borgiaa Department of Neurosciences , University of Padova , Italy.
Gianluca Sgarbib Department of Biomedical and Neuromotor Sciences , University of Bologna , Italy.
Giancarlo Solainib Department of Biomedical and Neuromotor Sciences , University of Bologna , Italy.
Ian J Holtc Medical Research Council, Mill Hill Laboratory , London , United Kingdom.
Antonella Spinazzolac Medical Research Council, Mill Hill Laboratory , London , United Kingdom.
Egle Perissinottod Department of Cardiac, Thoracic and Vascular Sciences, Biostatistics, Epidemiology and Public Health Unit , University of Padova , Padova , Italy.
Marco Sandrie Department of Biomedical Sciences , University of Padova , Italy.
Alessandra Baraccab Department of Biomedical and Neuromotor Sciences , University of Bologna , Italy.
Lodovica Vergania Department of Neurosciences , University of Padova , Italy.

Funding

Medical Research Council MC_ PC_ 13029Medical Research Council MC_PC_13029/1Medical Research Council MC_PC_13029/2
6 · The paper itself

Abstract

Pathological mutations in the mitochondrial DNA (mtDNA) produce a diverse range of tissue-specific diseases and the proportion of mutant mitochondrial DNA can increase or decrease with time via segregation, dependent on the cell or tissue type. Previously we found that adenocarcinoma (A549.B2) cells favored wild-type (WT) mtDNA, whereas rhabdomyosarcoma (RD.Myo) cells favored mutant (m3243G) mtDNA. Mitochondrial quality control (mtQC) can purge the cells of dysfunctional mitochondria via mitochondrial dynamics and mitophagy and appears to offer the perfect solution to the human diseases caused by mutant mtDNA. In A549.B2 and RD.Myo cybrids, with various mutant mtDNA levels, mtQC was explored together with macroautophagy/autophagy and bioenergetic profile. The 2 types of tumor-derived cell lines differed in bioenergetic profile and mitophagy, but not in autophagy. A549.B2 cybrids displayed upregulation of mitophagy, increased mtDNA removal, mitochondrial fragmentation and mitochondrial depolarization on incubation with oligomycin, parameters that correlated with mutant load. Conversely, heteroplasmic RD.Myo lines had lower mitophagic markers that negatively correlated with mutant load, combined with a fully polarized and highly fused mitochondrial network. These findings indicate that pathological mutant mitochondrial DNA can modulate mitochondrial dynamics and mitophagy in a cell-type dependent manner and thereby offer an explanation for the persistence and accumulation of deleterious variants.

Indexed as

A549 CellsAutophagyCytoplasmDNA, MitochondrialEnergy MetabolismHumansMicrotubule-Associated ProteinsMitochondriaMitophagyMutationOligomycinsSequestosome-1 ProteinDNA, MitochondrialMAP1LC3A protein, humanMicrotubule-Associated ProteinsOligomycinsSequestosome-1 ProteinSQSTM1 protein, humanA549.B2 adenocarcinoma cellsautophagymitochondriamitochondrial dynamicsmitochondrial quality controlmitophagymutation-m3243Gpathological mtDNARD.Myo rhabdomyosarcoma cells

Identifiers

PMID27627835
PMCPMC5103342

What Socratic 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 Socratic graph.