Magnesium is one of the most abundant intracellular cations, yet its role in liver biology has remained largely overlooked. Traditionally viewed as a passive enzymatic cofactor, magnesium is now emerging as a dynamic regulator of cellular signaling, mitochondrial function, and metabolic homeostasis.

In this talk, we will explore the hypothesis that magnesium is not merely a supporting player in hepatic physiology, but a central determinant of liver health and disease. I will discuss how alterations in magnesium transporters reshape intracellular ion balance, influence metabolic fluxes, and contribute to the progression of liver diseases, including steatotic and inflammatory conditions.

By integrating insights from ion transport biology, metabolic regulation, and disease modeling, we propose a new framework in which magnesium transport acts as a regulatory axis linking nutrient stress to hepatic dysfunction.

Rethinking magnesium as a signaling entity rather than a simple ion opens new conceptual and therapeutic perspectives in liver disease.