Evidence map›Paper›PMID 36189806›Full record

ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2022

How cytoskeletal proteins regulate mitochondrial energetics in cell physiology and diseases.

Tanya Solomon, Megha Rajendran, Tatiana Rostovtseva, Livia Hool

Open access · hybridAbstract readReview
In one paragraph

Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. In search of epigenetic hallmarks of different tissues: an integrative omics study of horse liver, lung, and heart.Mammalian genome : official journal of the International Mammalian Genome Society · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Cytoskeleton Rearrangement in Podocytopathies: An Update.International journal of molecular sciences · 2024
    Review
  10. Article
  11. Article
  12. Article
  13. 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

4 authors at 2 institutions in 2 countries.

Tanya SolomonSchool of Human Sciences, The University of Western Australia, Crawley, Western Australia, Australia.ORCID 0000-0001-7762-9809
Megha RajendranEunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
Tatiana RostovtsevaEunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.
Livia HoolSchool of Human Sciences, The University of Western Australia, Crawley, Western Australia, Australia.
National Institutes of Health · USThe University of Western Australia · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mitochondria are ubiquitous organelles that play a pivotal role in the supply of energy through the production of adenosine triphosphate in all eukaryotic cells. The importance of mitochondria in cells is demonstrated in the poor survival outcomes observed in patients with defects in mitochondrial gene or RNA expression. Studies have identified that mitochondria are influenced by the cell's cytoskeletal environment. This is evident in pathological conditions such as cardiomyopathy where the cytoskeleton is in disarray and leads to alterations in mitochondrial oxygen consumption and electron transport. In cancer, reorganization of the actin cytoskeleton is critical for trans-differentiation of epithelial-like cells into motile mesenchymal-like cells that promotes cancer progression. The cytoskeleton is critical to the shape and elongation of neurons, facilitating communication during development and nerve signalling. Although it is recognized that cytoskeletal proteins physically tether mitochondria, it is not well understood how cytoskeletal proteins alter mitochondrial function. Since end-stage disease frequently involves poor energy production, understanding the role of the cytoskeleton in the progression of chronic pathology may enable the development of therapeutics to improve energy production and consumption and slow disease progression. This article is part of the theme issue 'The cardiomyocyte: new revelations on the interplay between architecture and function in growth, health, and disease'.

Indexed as

Cytoskeletal ProteinsNeoplasmsAdenosine TriphosphateCell Physiological PhenomenaHumansMitochondriaRNAAdenosine TriphosphateCytoskeletal ProteinsRNAadenosine triphosphatecytoskeletonmetabolic activitymitochondrianetworkvoltage-dependent anion channel

Identifiers

PMID36189806
PMCPMC9527905
OpenAlexW4300690704

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.