Treatment with the mitochondrial-targeted antioxidant mitoTEMPO improves cardiac diastolic function, increases ATP levels, and reduces S-glutathionylation of cardiac myosin binding protein C (cMyBPC) in magnesium-deficient mice, indicating that mitochondrial oxidative stress mediates cardiomyopathy induced by magnesium deficiency.

When the body doesn't get enough magnesium, heart muscle cells have less magnesium inside them. This makes the energy-producing parts of the cell (mitochondria) work badly, so they release harmful chemicals and make less energy. These harmful chemicals attach to a protein that helps the heart muscle relax, changing it in a way that makes the heart stiff and not relax properly. An antioxidant that targets the mitochondria can block these harmful chemicals, restoring energy production and preventing the protein change, so the heart can relax better.