This is the authors' abstract. We don't add key points for this paper.
Cannabidiol (CBD) is a popular non-psychoactive formulation commonly used to treat pain, anxiety, and nausea. Currently, CBD has little to no regulatory oversight in the United States thus, inconsistencies exist regarding how CBD is produced and controlled. Moreover, little is known about its precise biological impact on cells and tissues, particularly in the kidney. To address this, we utilized human immortalized podocytes treated with varying concentrations of CBD for different durations, and assessed their intracellular calcium changes, mitochondrial bioenergetic changes, and viability. We demonstrate for the first time that prolonged exposure to CBD induces a dose-dependent elevation in intracellular Ca 2+ concentration and a decrease in mitochondrial bioenergetics, leading to cell damage and death. These findings identify mitochondrial bioenergetic impairment via calcium dysregulation as a key mechanism underlying CBD-induced podocyte cytotoxicity. Importantly, our results suggest that high-dose, long-term CBD exposure may compromise podocyte health and potentially impair kidney function. • CBD affects intracellular calcium handling in podocytes. • CBD causes mitochondrial bioenergetic impairments in podocytes. • High-dose CBD leads to cell injury and death in podocytes.
No takes yet. Share an insight, caveat, or question.
Didik et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: