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Cited by 159Mitochondrial Function and PathologyAutophagy in Disease and TherapyCellular transport and secretion

What is the function of mitochondrial networks? A theoretical assessment of hypotheses and proposal for future research

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Hoitzing, Hanne, Johnston, Iain G., Jones, Nick S.·2015·BioEssays
DOI 10.1002/bies.201400188PMC PMC4672710
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Abstract

Mitochondria can change their shape from discrete isolated organelles to a large continuous reticulum. The cellular advantages underlying these fused networks are still incompletely understood. In this paper, we describe and compare hypotheses regarding the function of mitochondrial networks. We use mathematical and physical tools both to investigate existing hypotheses and to generate new ones, and we suggest experimental and modelling strategies. Among the novel insights we underline from this work are the possibilities that (i) selective mitophagy is not required for quality control because selective fusion is sufficient; (ii) increased connectivity may have non‐linear effects on the diffusion rate of proteins; and (iii) fused networks can act to dampen biochemical fluctuations. We hope to convey to the reader that quantitative approaches can drive advances in the understanding of the physiological advantage of these morphological changes.

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  • The mitochondrial network in APOE4 astrocytes is in a static hyperfused state, with less fission/degradation and reduced mitochondrial biogenesis.

    “suggesting that their mitochondrial network is in a static hyperfused state49; i.e., less fission/degradation occurs together with reduced mitochondrial biogenesis.”

    From Altered mitochondrial dynamics and function in APOE4-expressing astrocytes (2020) · cites this paper as [49]

    In “Quantitative definitions of micro, meso- and hyperfusion” (page unavailable), the paper defines static hyperfusion as a highly fused state with rare or almost no fission events. It does not establish that APOE4 astrocytes are in that state or that they have reduced mitochondrial degradation and biogenesis. (LLM, conf=0.87)

    Experimental — accuracy not yet measured

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Authors
Hoitzing, H., Johnston, I. G., & Jones, N. S.
Affiliations
Imperial College London (GB)
Corresponding author
Jones, Nick S.
ORCID
Venue
BioEssays
Publisher
Wiley
Published
2015-04-03
Volume
37
Issue
6
Pages
687-700
ISSN
  • 0265-9247 (ISSN-L)
  • 1521-1878
DOI
10.1002/bies.201400188
PMC
PMC4672710
OpenAlex
W2056425757
Cited by
159
References
121
Citations by year
2026: 9 · 2025: 11 · 2024: 17 · 2023: 17 · 2022: 11 · 2021: 21 · 2020: 18 · 2019: 15 · 2018: 11 · 2017: 16 · 2016: 10 · 2015: 3
FWCI
1.30
Type
journal article
Language
en
Open access
Licence
Locations
  • BioEssays (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • University of Birmingham Research Portal (University of Birmingham) (submittedVersion)
  • Spiral (Imperial College London) (submittedVersion, other-oa)
Funders
  • BBSRC (BBD0201901)
  • MRC (MR/J013617/1)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
Keywords
mitochondrial network, mitochondrial fusion, mitochondrial morphology, mitochondrial quality control, protein diffusion, network connectivity
MeSH terms
Animals, Energy Metabolism, Humans, Mitochondria, Electron Transport Chain Complex Proteins, Mitochondrial Dynamics, Mitophagy

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