Evidence map›Paper›PMID 21967640›Full record

ReviewAntioxidants & redox signaling2012

Mitochondrial regulation of cell cycle and proliferation.

Valeria Gabriela Antico Arciuch, María Eugenia Elguero, Juan José Poderoso, María Cecilia Carreras

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 226 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
226citing papers in PubMed, 2 pooled it
–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

226 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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166 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

4 authors.

Valeria Gabriela Antico ArciuchLaboratory of Oxygen Metabolism, University of Buenos Aires, University Hospital, Argentina.
María Eugenia Elguero
Juan José Poderoso
María Cecilia Carreras

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Eukaryotic mitochondria resulted from symbiotic incorporation of α-proteobacteria into ancient archaea species. During evolution, mitochondria lost most of the prokaryotic bacterial genes and only conserved a small fraction including those encoding 13 proteins of the respiratory chain. In this process, many functions were transferred to the host cells, but mitochondria gained a central role in the regulation of cell proliferation and apoptosis, and in the modulation of metabolism; accordingly, defective organelles contribute to cell transformation and cancer, diabetes, and neurodegenerative diseases. Most cell and transcriptional effects of mitochondria depend on the modulation of respiratory rate and on the production of hydrogen peroxide released into the cytosol. The mitochondrial oxidative rate has to remain depressed for cell proliferation; even in the presence of O₂, energy is preferentially obtained from increased glycolysis (Warburg effect). In response to stress signals, traffic of pro- and antiapoptotic mitochondrial proteins in the intermembrane space (B-cell lymphoma-extra large, Bcl-2-associated death promoter, Bcl-2 associated X-protein and cytochrome c) is modulated by the redox condition determined by mitochondrial O₂ utilization and mitochondrial nitric oxide metabolism. In this article, we highlight the traffic of the different canonical signaling pathways to mitochondria and the contributions of organelles to redox regulation of kinases. Finally, we analyze the dynamics of the mitochondrial population in cell cycle and apoptosis.

Indexed as

Cell CycleAnimalsCell DeathCell ProliferationHumansMitochondriaOxidation-ReductionPhosphotransferasesReactive Oxygen SpeciesSignal TransductionPhosphotransferasesReactive Oxygen Species

Identifiers

PMID21967640
PMCPMC3315176

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.