Evidence map›Paper›PMID 25678368›Full record

ArticleBiotechnology and bioengineering2015

Automated detection of whole-cell mitochondrial motility and its dependence on cytoarchitectural integrity.

Judith Kandel, Philip Chou, David M Eckmann

Abstract read
In one paragraph

Article in Biotechnology and bioengineering, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  8. Article
  9. How cytoskeletal proteins regulate mitochondrial energetics in cell physiology and diseases.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2022
    Review
  10. Review
  11. Article
  12. Crosstalk between mechanotransduction and metabolism.Nature reviews. Molecular cell biology · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Translational Application of Measuring Mitochondrial Functions in Blood Cells Obtained from Patients with Acute Poisoning.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2018
    Article
  19. Article
  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 2 institutions in 1 country.

Judith KandelDepartment of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania, 19104.
Philip ChouDepartment of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania, 19104.
David M EckmannDepartment of Bioengineering, University of Pennsylvania, Philadelphia, Pennsylvania, 19104. david.eckmann@uphs.upenn.edu.
University of Pennsylvania · USUniversity City Science Center · US

Funding

Multidisciplinary Training in Cardiovascular BiologyT32HL007954 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI DAVIES, PETER FRANCIS · 2000 to 2019
$9.9M
NHLBI NIH HHS T32 HL007954
6 · The paper itself

Abstract

Current methodologies used for mitochondrial motility analysis tend to either overlook individual mitochondrial tracks or analyze only peripheral mitochondria instead of mitochondria in all regions of the cell. Furthermore, motility analysis of an individual mitochondrion is usually quantified by establishing an arbitrary threshold for "directed" motion. In this work, we created a custom, publicly available computational algorithm based on a previously published approach (Giedt et al., 2012. Ann Biomed Eng 40:1903-1916) in order to characterize the distribution of mitochondrial movements at the whole-cell level, while still preserving information about single mitochondria. Our technique is easy to use, robust, and computationally inexpensive. Images are first pre-processed for increased resolution, and then individual mitochondria are tracked based on object connectivity in space and time. When our method is applied to microscopy fields encompassing entire cells, we reveal that the mitochondrial net distances in fibroblasts follow a lognormal distribution within a given cell or group of cells. The ability to model whole-cell mitochondrial motility as a lognormal distribution provides a new quantitative paradigm for comparing mitochondrial motility in naïve and treated cells. We further demonstrate that microtubule and microfilament depolymerization shift the lognormal distribution in directions which indicate decreased and increased mitochondrial movement, respectively. These findings advance earlier work on neuronal axons (Morris and Hollenbeck, 1993. J Cell Sci 104:917-927) by relating them to a different cell type, applying them on a global scale, and automating measurement of mitochondrial motility in general.

Indexed as

Cell Physiological PhenomenaMovementActin CytoskeletonAlgorithmsCells, CulturedComputational BiologyCytological TechniquesFibroblastsHumansMitochondriacytoskeletonmicrofilamentsmicrotubulesmitochondrial motilitysingle particle tracking

Identifiers

PMID25678368
PMCPMC4452426
OpenAlexW1920464377

What OpenQuestion holds

Textmetadata
LicenceTDM
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.