What topics does this cannabis study cover?

This study covers research on: CBD, Inflammation, Endocannabinoid.

Where was this research published?

Published in Redox biology on August 5, 2026.

CBD may curb heart scarring in Duchenne muscular dystrophy cells

Q: What did this research study find?

*CBD* **reduced TGF-β-induced myofibroblast activation** in heart fibroblast cells from both healthy controls and people with DMD.

Cannabidiol-induced Heme oxygenase-1 contributes to modulate the phenotype of hiPSC-derived cardiac fibroblasts from patients with Duchenne muscular dystrophy.

Redox biology • August 5, 2026 • Highly Relevant

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AI Summary

This laboratory study examined how cannabidiol (CBD) affects heart fibroblast cells made from human stem cells, including cells from people with Duchenne muscular dystrophy (DMD). Although CBD changed energy use in healthy cells by promoting glycolysis and cell growth, these metabolic effects were not seen in DMD-derived cells. The study did not report clinical results in people, so it cannot show that CBD treats DMD or prevents heart complications in patients.

In both healthy and DMD-derived cells, CBD reduced the transformation of fibroblasts into myofibroblasts—cells strongly linked to scar formation—after exposure to the profibrotic signal TGF-β. It also reduced oxidative stress and increased the antioxidant protein heme oxygenase-1 (HO-1). Blocking HO-1 weakened CBD’s anti-fibrotic effect, suggesting that HO-1 is a key pathway through which CBD may limit cardiac fibrosis. These findings are promising for future research, but they come from a cell model and do not establish a safe or effective cannabis-based treatment for people with DMD.

💡 Key Findings

CBD reduced TGF-β-induced myofibroblast activation in heart fibroblast cells from both healthy controls and people with DMD.

Moderate

50%

CBD produced strong antioxidant effects, including reduced intracellular reactive oxygen species and increased glutathione levels in both cell groups.

Moderate

50%

The study identified HO-1 as a key mediator of CBD’s anti-fibrotic action: inhibiting HO-1 weakened CBD’s ability to suppress fibroblast activation.

Moderate

50%

CBD promoted glycolysis and cell proliferation in control cells, but the glycolytic response was not observed in DMD-derived cells.

Moderate

50%

📄 Original Abstract

Duchenne muscular dystrophy (DMD) is a severe and progressive form of muscular dystrophy caused by mutations in the dystrophin gene. We previously observed that loss of dystrophin in human induced pluripotent stem cell-derived cardiac fibroblasts (hiPSC-cFib) dysregulated the actin network and induced a metabolic remodeling associated with an exacerbated myofibroblast phenotype. The endocannabinoid signaling (ECS) system plays an important role in chronic inflammatory and fibrotic conditions and is dysregulated in skeletal muscle of DMD patients. Here, we investigated the effects of cannabidiol (CBD) on hiPSC-cFib from healthy controls and DMD patients. CBD failed to modify metabolic responses in DMD hiPSC-cFib, while significantly promoting glycolysis and cell proliferation in control hiPSC-cFib. Despite these distinct metabolic responses, CBD significantly attenuated TGF-β-induced myofibroblast activation in both DMD and control hiPSC-cFib by lowering α-smooth muscle actin and collagen type I levels suggesting a metabolism-independent mechanism. Additionally, CBD exerted strong antioxidant effects on both DMD and control hiPSC-cFib, markedly reducing intracellular reactive oxygen species (ROS) levels, increasing GSH levels and robustly inducing heme oxygenase-1 (HO-1) expression in a time- and dose-dependent manner which could not be mimicked by CB1R or CB2R agonists and blocked by their antagonists. Pharmacological inhibition of HO-1 blunted CBD's ability to suppress TGF-β-induced activation of DMD and control hiPSC-cFib, demonstrating that HO-1 is a key mediator of CBD's anti-fibrotic action. Together, these findings showed stimulation of glycolytic metabolism by CBD, regulation which is lost in DMD hiPSC-cFib. We uncovered a previously unrecognized HO-1-dependent pathway by which CBD dampens profibrotic activation in human DMD and control hiPSC-cFib, highlighting its potential as a therapeutic approach to limit cardiac fibrosis in Duchenne muscular dystrophy.

Paper Type

📄 Research

Publication

Journal: Redox biology
Published: August 5, 2026
PMID: 42579928
DOI: 10.1016/j.redox.2026.104333

Authors (10)

L Savchenko Institut des Maladies Métaboliques et Cardiovasculaires I2MC, Toulouse, France.
S Soussi Institut des Maladies Métaboliques et Cardiovasculaires I2MC, Toulouse, France.
D Rovina Unit of Inherited Cardiomyopathies, Centro Cardiologico Monzino IRCCS, Milan, Italy.
A Swiader Institut des Maladies Métaboliques et Cardiovasculaires I2MC, Toulouse, France.
S Mallia Unit of Inherited Cardiomyopathies, Centro Cardiologico Monzino IRCCS, Milan, Italy.
+5 more authors