Evidence map›Paper›PMID 39187541›Full record

ArticleScientific reports2024

Detailed analysis of Mdivi-1 effects on complex I and respiratory supercomplex assembly.

Nico Marx, Nadine Ritter, Paul Disse, Guiscard Seebohm, Karin B Busch

Abstract read
In one paragraph

Article in Scientific reports, 2024. 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
–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

24 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Review
  17. Mitochondria as a Therapeutic Target in Metabolic Disorders.Mini reviews in medicinal chemistry · 2026
    Review
  18. 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

5 authors.

Nico MarxDepartment of Biology, Institute of Integrative Cell Biology and Physiology (IIZP), University of Münster, Schloßplatz 5, 48149, Münster, Germany.
Nadine RitterDepartment of Cardiovascular Medicine, Institute for Genetics of Heart Diseases (IfGH), University Hospital Münster, 48149, Münster, Germany.
Paul DisseDepartment of Cardiovascular Medicine, Institute for Genetics of Heart Diseases (IfGH), University Hospital Münster, 48149, Münster, Germany.
Guiscard SeebohmDepartment of Cardiovascular Medicine, Institute for Genetics of Heart Diseases (IfGH), University Hospital Münster, 48149, Münster, Germany.
Karin B BuschDepartment of Biology, Institute of Integrative Cell Biology and Physiology (IIZP), University of Münster, Schloßplatz 5, 48149, Münster, Germany. buschkar@uni-muenster.de.

Funding

Deutsche Forschungsgemeinschaft SFB944, project number 180879236
6 · The paper itself

Abstract

Several human diseases, including cancer and neurodegeneration, are associated with excessive mitochondrial fragmentation. In this context, mitochondrial division inhibitor (Mdivi-1) has been tested as a therapeutic to block the fission-related protein dynamin-like protein-1 (Drp1). Recent studies suggest that Mdivi-1 interferes with mitochondrial bioenergetics and complex I function. Here we show that the molecular mechanism of Mdivi-1 is based on inhibition of complex I at the IQ site. This leads to the destabilization of complex I, impairs the assembly of N- and Q-respirasomes, and is associated with increased ROS production and reduced efficiency of ATP generation. Second, the calcium homeostasis of cells is impaired, which for example affects the electrical activity of neurons. Given the results presented here, a potential therapeutic application of Mdivi-1 is challenging because of its potential impact on synaptic activity. Similar to the Complex I inhibitor rotenone, Mdivi-1 may lead to neurodegenerative effects in the long term.

Indexed as

Electron Transport Complex IMitochondriaQuinazolinonesAdenosine TriphosphateAnimalsCalciumHumansMiceMitochondrial DynamicsNeuronsReactive Oxygen Species3-(2,4-dichloro-5-methoxyphenyl)-2-sulfanyl-4(3H)-quinazolinoneAdenosine TriphosphateCalciumElectron Transport Complex IQuinazolinonesReactive Oxygen SpeciesCalcium metabolismInhibitionMdivi-1MitochondriaNeuronal activityRespiratory complex IRespiratory supercomplexes

Identifiers

PMID39187541
PMCPMC11347648

What Socratic 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 Socratic graph.