Evidence map›Paper›PMID 25997954›Full record

ReviewMedical science monitor : international medical journal of experimental and clinical research2015

Hypoxia defined as a common culprit/initiation factor in mitochondrial-mediated proinflammatory processes.

George B Stefano, Richard M Kream

Open access · hybridAbstract readReview
In one paragraph

Review in Medical science monitor : international medical journal of experimental and clinical research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.8field-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

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Behaviorally-Mediated Entrainment of Whole-Body Metabolic Processes: Conservation and Evolutionary Development of Mitochondrial Respiratory Complexes.Medical science monitor : international medical journal of experimental and clinical research · 2019
    Article
  5. Review
  6. Microbiome and Health: Ramifications of Intelligent Deception.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  7. Microbiome: A Potential Component in the Origin of Mental Disorders.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Review
  8. Aging Reversal and Healthy Longevity is in Reach: Dependence on Mitochondrial DNA Heteroplasmy as a Key Molecular Target.Medical science monitor : international medical journal of experimental and clinical research · 2017
    Review
  9. Review
  10. Review
  11. Glycolytic Coupling to Mitochondrial Energy Production Ensures Survival in an Oxygen Rich Environment.Medical science monitor : international medical journal of experimental and clinical research · 2016
    Review
  12. Article
  13. Review
  14. Cancer: Mitochondrial Origins.Medical science monitor : international medical journal of experimental and clinical research · 2015
    Review
  15. Mitochondria, Chloroplasts in Animal and Plant Cells: Significance of Conformational Matching.Medical science monitor : international medical journal of experimental and clinical research · 2015
    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

2 authors.

George B StefanoMitoGenetics, LLC, Farmingdale, NY, USA.
Richard M KreamMitoGenetics, LLC, Farmingdale, NY, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In mammals and invertebrates, the activities of neuro- and immuno-competent cells, e.g., glia, which are present in nervous tissues, are deemed of critical importance to normative neuronal function. The responsiveness of invertebrate and vertebrate immuno-competent glia to a common set of signal molecules, such as nitric oxide and endogenous morphine, is functionally linked to physiologically driven innate immunological and neuronal activities. Importantly, the presence of a common, evolutionarily conserved, set of signal molecules in comparative animal groups strongly suggests an expansive intermediate metabolic profile dependent on high output mitochondrial ATP production and utilization. Normative bidirectional neural-immune communication across invertebrate and vertebrate species requires common anatomical and biochemical substrates and pathways involved in energy production and mitochondrial integrity. Within this closed-loop system, abnormal perturbation of the respective tissue functions will have profound ramifications in functionally altering associated nervous and vascular systems and it is highly likely that the initial trigger to the induction of a physiologically debilitating pro-inflammatory state is a micro-environmental hypoxic event. This is surmised by the need for an unwavering constant oxygen supply. In this case, temporal perturbations of normative oxygen tension may be tolerated for short, but not extended, periods and ischemic/hypoxic perturbations in oxygen delivery represent significant physiological challenges to overall cellular and multiple organ system viability. Hence, hypoxic triggering of multiple pro-inflammatory events, if not corrected, will promote pathophysiological amplification leading to a deleterious cascade of bio-senescent cellular and molecular signaling pathways, which converge to markedly impair mitochondrial energy utilization and ATP production.

Indexed as

Models, BiologicalAdenosine TriphosphateAnimalsBiological EvolutionCell HypoxiaCellular MicroenvironmentCellular SenescenceCytokinesEnergy MetabolismGene Expression RegulationHumansImmunity, InnateImmunocompetenceInflammationInvertebratesMicrogliaAdenosine TriphosphateCytokinesNitric OxideNitritesOpioid Peptides

Identifiers

PMID25997954
PMCPMC4451716
OpenAlexW1934820269

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.