Evidence map›Paper›PMID 10535904›Full record

ReviewProceedings of the National Academy of Sciences of the United States of America1999

The metabolic implications of intracellular circulation.

P W Hochachka

Abstract readReview
In one paragraph

Review in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing 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

30 citing papers in PubMed.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Structural characterization of carangid fish myoglobins.Fish physiology and biochemistry · 2012
    Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Order without design.Theoretical biology & medical modelling · 2010
    Review
  14. Review
  15. Strong inference for systems biology.PLoS computational biology · 2009
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Microfluidics of cytoplasmic streaming and its implications for intracellular transport.Proceedings of the National Academy of Sciences of the United States of America · 2008
    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

1 author.

P W HochachkaDepartment of Zoology, University of British Columbia, Vancouver, BC Canada V6T 1Z4. PWH@zoology.ubc.ca

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Two views currently dominate research into cell function and regulation. Model I assumes that cell behavior is quite similar to that expected for a watery bag of enzymes and ligands. Model II assumes that three-dimensional order and structure constrain and determine metabolite behavior. A major problem in cell metabolism is determining why essentially all metabolite concentrations are remarkably stable (are homeostatic) over large changes in pathway fluxes-for convenience, this is termed the [s] stability paradox. For muscle cells, ATP and O(2) are the most perfectly homeostatic, even though O(2) delivery and metabolic rate correlate in a 1:1 fashion. In total, more than 60 metabolites are known to be remarkably homeostatic in differing metabolic states. Several explanations of [s] stability are usually given by traditional model I studies-none of which apply to all enzymes in a pathway, and all of which require diffusion as the means for changing enzyme-substrate encounter rates. In contrast, recent developments in our understanding of intracellular myosin, kinesin, and dyenin motors running on actin and tubulin tracks or cables supply a mechanistic basis for regulated intracellular circulation systems with cytoplasmic streaming rates varying over an approximately 80-fold range (from 1 to >80 micrometer x sec(-1)). These new studies raise a model II hypothesis of intracellular perfusion or convection as a primary means for bringing enzymes and substrates together under variable metabolic conditions. In this view, change in intracellular perfusion rates cause change in enzyme-substrate encounter rates and thus change in pathway fluxes with no requirement for large simultaneous changes in substrate concentrations. The ease with which this hypothesis explains the [s] stability paradox is one of its most compelling features.

Indexed as

HomeostasisAnimalsHumansMusclesOxygenPhosphatesSignal TransductionOxygenPhosphates

Identifiers

PMID10535904
PMCPMC34257

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.