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Research summary · AI summary · not yet reviewedAnimal studyCell studyInterventionalPublished in a peer-reviewed journal
Effect of Dimethyl Fumarate on Diabetic db/db Mice Aortas and HUVECs
In a study involving diabetic db/db mice and human umbilical vein endothelial cells (HUVECs), Dimethyl Fumarate (DMF) improved endothelial function by restoring endothelium-dependent relaxations in mouse aortas and mesenteric arteries. DMF also enhanced glucose tolerance and reduced mitochondrial ROS and inflammatory markers. However, these protective effects diminished when TFEB was knocked down.
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This plain-English summary was written by AI from a published abstract and may contain errors. It is not medical advice. Read the original study and talk to your MS team before making decisions about treatment.
- Human efficacy
- Not yet tested in people
- Mechanism
- Other
- Evidence strength
- Early – laboratory or animal research
- Outcome
- Positive
Results in cells or animals often do not carry over to people with MS.
Why it matters
These findings suggest that DMF may combat endothelial dysfunction in diabetes through targeting the TFEB pathway, potentially offering insights for future therapeutic strategies.
What this does not prove
The study did not investigate the long-term effects of DMF on endothelial function after treatment, which limits understanding of its sustained efficacy.
Next milestone
No next milestone was established from the available source.
Study facts
- Study design
- Interventional
- Participants / samples
- Not reported
- Randomised
- Not reported
- Controlled
- Not reported
- Primary endpoint met
- Not reported
- Relevant MS type
- Not reported
- Publication date
- 2026-10-30
- Evidence reviewed
- Abstract only
- Regulatory approval
- Yes
- Research areas
- Other
- Biological target
- TFEB
- Pathway
- Not reported
- Population
- Diabetic db/db mice and human umbilical vein endothelial cells (HUVECs)
- Size of effect
- Not reported
- Secondary endpoints
- Not reported
- MRI endpoints
- Not reported
- Biomarkers
- Not reported
- Safety
- Not reported
Original sources
- Primary evidenceTranscription factor EB as a novel target for dimethyl fumarate to restore endothelial function in diabetes. ↗DOI: 10.1038/s41401-026-01944-0
Supporting passages (16)
study phaseDimethyl fumarate (DMF), an FDA-approved drug for multiple sclerosis and psoriasis, exhibits potent anti-inflammatory and antioxidant properties, yet whether it protects against diabetic endothelial dysfunction and the underlying molecular mechanisms remain unclear.
study designHere, diabetic db/db mice and the non-diabetic db/m+ littermates were treated with DMF (100 mg·kg-1·d-1) or vehicle for 4 weeks, and vascular function in aortic and mesenteric artery rings was assessed by wire myography.
subjectstreated with DMF (100 mg·kg-1·d-1) or vehicle for 4 weeks, and vascular function in aortic and mesenteric artery rings was assessed by wire myography.
speciesHuman umbilical vein endothelial cells (HUVECs) and endothelial cell (EC)-specific Tfeb knockout (TfebECKO) mice were employed to investigate the target of DMF in vitro and in vivo.
regulatory approvalDimethyl fumarate (DMF), an FDA-approved drug for multiple sclerosis and psoriasis, exhibits potent anti-inflammatory and antioxidant properties, yet whether it protects against diabetic endothelial dysfunction and the underlying molecular mechanisms remain unclear.
research categoriesDimethyl fumarate (DMF), an FDA-approved drug for multiple sclerosis and psoriasis, exhibits potent anti-inflammatory and antioxidant properties, yet whether it protects against diabetic endothelial dysfunction and the underlying molecular mechanisms remain unclear.
publication date2026-10-30
primary endpointassessed by wire myography.
findingsTogether, DMF ameliorates endothelial dysfunction in diabetes by inhibiting TFEB phosphorylation and restoring TFEB nuclear activity.
mechanismsThese protective effects of DMF were largely reversed by TFEB knockdown in HUVECs or in aortas of TfebECKO mice.
biological targetsimplicating a role of TFEB in DMF-induced suppression of inflammatory and oxidative pathways.
populationHuman umbilical vein endothelial cells (HUVECs) and endothelial cell (EC)-specific Tfeb knockout (TfebECKO) mice were employed to investigate the target of DMF in vitro and in vivo.
outcomeDMF restored the impaired endothelium-dependent relaxations (EDRs) in db/db mouse aortas and insulin-induced relaxations in mesenteric arteries, improved glucose tolerance, reduced aortic endothelial mitochondrial ROS (mito-ROS) accumulation, and lowered the expression of inflammatory markers.
limitationsTitle: Transcription factor EB as a novel target for dimethyl fumarate to restore endothelial function in diabetes.
peer reviewedPublication types: Journal Article
human efficacytreated with DMF (100 mg·kg-1·d-1) or vehicle for 4 weeks, and vascular function in aortic and mesenteric artery rings was assessed by wire myography.
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