Evidence map›Paper›PMID 24309936›Full record

ArticleCell death & disease2013

Direct modulation of the outer mitochondrial membrane channel, voltage-dependent anion channel 1 (VDAC1) by cannabidiol: a novel mechanism for cannabinoid-induced cell death.

N Rimmerman, D Ben-Hail, Z Porat, A Juknat, E Kozela, M P Daniels, P S Connelly, E Leishman, H B Bradshaw, V Shoshan-Barmatz and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

88 citing papers in PubMed, 160 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Cannabidiol-Ion Channel Interactions Represent a Promising Preventive and Therapeutic Strategy in Hepatocellular Carcinoma.Pathophysiology : the official journal of the International Society for Pathophysiology · 2026
    Review
  5. Article
  6. Article
  7. The effects of Cannabidiol on podocytes in vitro.Biochemical and biophysical research communications · 2025
    Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Advances and Challenges in Modeling Cannabidiol Pharmacokinetics and Hepatotoxicity.Drug metabolism and disposition: the biological fate of chemicals · 2024
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article

28 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

11 authors at 5 institutions in 2 countries.

N RimmermanThe Dr. Miriam and Sheldon G Adelson Center for the Biology of Addictive Diseases, Department of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
D Ben-Hail
Z Porat
A Juknat
E Kozela
M P Daniels
P S Connelly
E Leishman
H B Bradshaw
V Shoshan-Barmatz
Z Vogel
Tel Aviv University · ILBen-Gurion University of the Negev · ILIndiana University Bloomington · USNational Heart Lung and Blood Institute · USWeizmann Institute of Science · IL

Funding

Electron Microscopy CoreZICHL005906 · NHLBI · NATIONAL HEART, LUNG, AND BLOOD INSTITUTE · PI SYED, ZULFEQHAR · 2009 to 2025
$12.9M
Microglial activation by N-arachidonoyl glycineR21DA032150 · NIDA · TRUSTEES OF INDIANA UNIVERSITY · PI BRADSHAW, HEATHER BRYTE · 2011 to 2012
$424k
NIDA NIH HHS R21 DA032150
6 · The paper itself

Abstract

Cannabidiol (CBD) is a non-psychoactive plant cannabinoid that inhibits cell proliferation and induces cell death of cancer cells and activated immune cells. It is not an agonist of the classical CB1/CB2 cannabinoid receptors and the mechanism by which it functions is unknown. Here, we studied the effects of CBD on various mitochondrial functions in BV-2 microglial cells. Our findings indicate that CBD treatment leads to a biphasic increase in intracellular calcium levels and to changes in mitochondrial function and morphology leading to cell death. Density gradient fractionation analysis by mass spectrometry and western blotting showed colocalization of CBD with protein markers of mitochondria. Single-channel recordings of the outer-mitochondrial membrane protein, the voltage-dependent anion channel 1 (VDAC1) functioning in cell energy, metabolic homeostasis and apoptosis revealed that CBD markedly decreases channel conductance. Finally, using microscale thermophoresis, we showed a direct interaction between purified fluorescently labeled VDAC1 and CBD. Thus, VDAC1 seems to serve as a novel mitochondrial target for CBD. The inhibition of VDAC1 by CBD may be responsible for the immunosuppressive and anticancer effects of CBD.

Indexed as

AnimalsBlotting, WesternCannabidiolCannabinoidsCell DeathCell LineFlow CytometryMiceMicrogliaVoltage-Dependent Anion Channel 1CannabidiolCannabinoidsVDAC1 protein, humanVoltage-Dependent Anion Channel 1

Identifiers

PMID24309936
PMCPMC3877544
OpenAlexW1992661831

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.