Evidence map›Paper›PMID 39420231›Full record

ReviewNature reviews. Molecular cell biology2025

Molecular mechanisms of mitochondrial dynamics.

Luis-Carlos Tábara, Mayuko Segawa, Julien Prudent

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature reviews. Molecular cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 225 papers.

0numbers the graph read from it
0cells of the map it votes in
225citing 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

225 citing papers in PubMed.

  1. Article
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  15. OPA1 controls mitochondrial dysfunction-driven liver fibrosis in MASLD.bioRxiv : the preprint server for biology · 2026
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

165 more citing papers are in PubMed but not listed here.

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.

Luis-Carlos Tábara *Medical Research Council Mitochondrial Biology Unit, University of Cambridge, Cambridge, UK.
Mayuko Segawa *Medical Research Council Mitochondrial Biology Unit, University of Cambridge, Cambridge, UK.ORCID http://orcid.org/0000-0002-5680-9576
Julien PrudentMedical Research Council Mitochondrial Biology Unit, University of Cambridge, Cambridge, UK. julien.prudent@mrc-mbu.cam.ac.uk.ORCID http://orcid.org/0000-0003-3821-6088

Funding

Medical Research Council MC_UU_00028/5
6 · The paper itself

Abstract

Mitochondria not only synthesize energy required for cellular functions but are also involved in numerous cellular pathways including apoptosis, calcium homoeostasis, inflammation and immunity. Mitochondria are dynamic organelles that undergo cycles of fission and fusion, and these transitions between fragmented and hyperfused networks ensure mitochondrial function, enabling adaptations to metabolic changes or cellular stress. Defects in mitochondrial morphology have been associated with numerous diseases, highlighting the importance of elucidating the molecular mechanisms regulating mitochondrial morphology. Here, we discuss recent structural insights into the assembly and mechanism of action of the core mitochondrial dynamics proteins, such as the dynamin-related protein 1 (DRP1) that controls division, and the mitofusins (MFN1 and MFN2) and optic atrophy 1 (OPA1) driving membrane fusion. Furthermore, we provide an updated view of the complex interplay between different proteins, lipids and organelles during the processes of mitochondrial membrane fusion and fission. Overall, we aim to present a valuable framework reflecting current perspectives on how mitochondrial membrane remodelling is regulated.

Indexed as

MitochondriaMitochondrial DynamicsAnimalsDynaminsGTP PhosphohydrolasesHumansMembrane FusionMitochondrial MembranesMitochondrial ProteinsDynaminsGTP PhosphohydrolasesMitochondrial Proteins

Identifiers

What Socratic 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 Socratic graph.