Cardiovascular disease and diabetes are often associated with each other, as many issues caused by diabetes promote heart issues. It stands to reason that perhaps a diabetes drug may be able to treat cardiovascular disease.
That is what a team from the Medical University at Innsbruck in Austria thought. The drug empagliflozin is an inhibitor of a protein called sodium-glucose transporter 2 (SGLT2) and is used to treat type 2 diabetes. Surprisingly, empagliflozin has also shown cardioprotective effects in several studies, leading some to wonder if it could be a preventative drug for cardiovascular disease.
The team decided to investigate empagliflozin’s effects as a cardioprotective agent and how it might conduct its protection. The team used a relatively short-term diabetic mouse model for this study, as long-term models can sometimes result in quite variable results.
The expected short-term effects of improved insulin sensitivity were clear from the beginning. Empagliflozin therapy also reduced inflammatory and cardiac fibrosis markers compared to controls. Inflammation can cause blood flow issues in the short term, with fibrosis being a cardiovascular disease where the heart progressively stiffens until heart failure occurs.
The team also observed that a protein marker of mitochondrial mass was upregulated in empagliflozin treated mice. Electron microscopy showed that the mitochondria in the treated mice were markedly different in their structures and size than control diabetic mice. Mitochondria are critical parts of the cell, so any such changes are a big deal.
This short study identified some possible mechanisms by which empagliflozin could act as a cardioprotective agent. The reduced protein inflammatory and fibrosis markers are the clearest sign of the cardioprotective effects of empagliflozin. The mitochondrial effects were interesting, as diabetes often causes abnormal mitochondrial structures. Empagliflozin may alleviate that abnormality to some degree, which could rescue endangered cells (or enable proper cell death if need be). This study wasn’t a comprehensive one, but never the less supplied some idea for future studies to work on.
The study concludes, “Mechanistically, improved mitochondrial ultrastructure, ameliorated over-activation of insulin signaling activity and changed macrophage polarization might contribute to cardioprotective effects of empagliflozin.”