“Heart failure (HF) is characterized by energy deprivation, calcium (Ca2+) handling alterations, and inflammation: effects associated with mitochondrial dysfunction.
Cannabidiol previously prevented mitochondrial dysfunction. Thus, it may prevent HF progression.
In mice with HF, subcutaneous cannabidiol attenuated cardiac fibrosis, hypertrophy, loss of ejection fraction, and inflammation; isolated cardiomyocytes preserved cell shortening, Ca2+ handling, mitochondrial function and redox balance. Hypertrophied ventricular cardiomyoblasts suggested cannabidiol-mediated effects through peroxisome proliferator-activated gamma receptors.
Therefore, cannabidiol in HF limited cardiac hypertrophy and preserved contractile function by sustaining cardiomyocyte and mitochondrial function through redox balance maintenance, supporting cannabidiol role as a cardioprotective therapy in HF.”
https://pubmed.ncbi.nlm.nih.gov/40562493/
“This study demonstrated that cannabidiol offers cardioprotection in a HF mouse model induced by L-NAME and ANGII administration. The results showed improved cardiac function and reduced cardiac hypertrophy, remodeling, inflammation, and cell death. In cardiomyocytes from the HF model, cannabidiol restored cell shortening, which was linked to improved calcium Ca2+ handling.
Additionally, it helped preserve cellular oxidative status, mitochondrial bioenergetics, and notably, modulated mCa2+ overload by affecting MCU expression. This suggests that the cardioprotective effects of cannabidiol are caused by the preservation of excitation-contraction-energetic coupling. The identified cellular mechanisms through which cannabidiol exerts its cardioprotective effects include reducing oxidative stress and the activation of PPAR-γ, which helps prevent mitochondrial dysfunction by decreasing MCU hyperactivity.”
“TRANSLATIONAL OUTLOOK: This study contributes to the knowledge of a novel therapy based on cannabidiol on the pathophysiology of HF, which is supported by preclinical data. Here, we described that cardioprotection exerted by cannabidiol on a HF mouse model was caused by the attenuation of cardiac fibrosis and hypertrophy along with improved ejection fraction and cardiac output. This was achieved, in the cardiomyocyte, by preservation of cell shortening, sarcoplasmic reticulum Ca2+ uptake, mitochondrial function, and redox balance, with data supporting the role of a PPAR-γ–dependent mechanism. This study suggests promising therapeutic results of cannabidiol used in the clinical field of HF treatment. In this regard, these results have inspired a translational effort to assess its effects in HF and cardiac dysfunction.”
