Evidence map›Paper›PMID 22901241›Full record

ReviewAntioxidants & redox signaling2013

Mitochondria-mediated energy adaption in cancer: the H(+)-ATP synthase-geared switch of metabolism in human tumors.

María Sánchez-Aragó, Laura Formentini, José M Cuezva

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

38 citing papers in PubMed, 61 citations in OpenAlex.

  1. Review
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  14. Effects of a Ketogenic Diet on [Molecular imaging and biology · 2019
    Article
  15. Article
  16. Article
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  18. The Role of Mitochondrial HFrontiers in oncology · 2018
    Review
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  20. 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

3 authors at 1 institution in 1 country.

María Sánchez-AragóDepartamento de Biología Molecular, Centro de Biología Molecular Severo Ochoa, Centro de Investigación Biomédica en Red de Enfermedades Raras, Centro de Investigación Hospital 12 de Octubre, Madrid, Spain.
Laura Formentini
José M Cuezva
Centro de Investigación Biomédica en Red · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

significanceSince the signing of the National Cancer Act in 1971, cancer still remains a major cause of death despite significant progresses made in understanding the biology and treatment of the disease. After many years of ostracism, the peculiar energy metabolism of tumors has been recognized as an additional phenotypic trait of the cancer cell. RECENT ADVANCES: While the enhanced aerobic glycolysis of carcinomas has already been translated to bedside for precise tumor imaging and staging of cancer patients, accepting that an impaired bioenergetic function of mitochondria is pivotal to understand energy metabolism of tumors and in its progression is debated. However, mitochondrial bioenergetics and cell death are tightly connected. CRITICAL ISSUES: Recent clinical findings indicate that H(+)-ATP synthase, a core component of mitochondrial oxidative phosphorylation, is repressed at both the protein and activity levels in human carcinomas. This review summarizes the relevance that mitochondrial function has to understand energy metabolism of tumors and explores the connection between the bioenergetic function of the organelle and the activity of mitochondria as tumor suppressors. FUTURE DIRECTIONS: The reversible nature of energy metabolism in tumors highlights the relevance that the microenvironment has for tumor progression. Moreover, the stimulation of mitochondrial activity or the inhibition of glycolysis suppresses tumor growth. Future research should elucidate the mechanisms promoting the silencing of oxidative phosphorylation in carcinomas. The aim is the development of new therapeutic strategies tackling energy metabolism to eradicate tumors or at least, to maintain tumor dormancy and transform cancer into a chronic disease.

Indexed as

Energy MetabolismAnimalsCarcinomaCell DeathHumansMitochondriaMitochondrial Proton-Translocating ATPasesNeoplasmsOxidative PhosphorylationTumor MicroenvironmentTumor Suppressor ProteinsMitochondrial Proton-Translocating ATPasesTumor Suppressor Proteins

Identifiers

PMID22901241
PMCPMC3691914
OpenAlexW2056420027

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.