Aortic Stenosis, Treated with Medicines, Not Surgery [Science Now]

Aortic valve stenosis is a disease in which the aortic valve of the heart gradually calcifies due to aging and fails to function normally. In severe cases, it can lead to heart failure. Since



there is no drug treatment available yet, the only treatment options are open chest surgery or TAVI, which involves inserting a stent to replace the aortic valve.



Recently, a domestic research team announced the results of a study showing that 'spermidine', which is attracting attention as one of the anti-aging substances, can inhibit the progression of aortic valve stenosis. This is the first study result suggesting the possibility of treating aortic valve stenosis with drugs.



Professor Lee Sa-min of the Department of Cardiology at Seoul Asan Medical Center is treating a patient with aortic valve stenosis [Photo = Seoul Asan Medical Center]



Professor Lee Sa-min's team of the Department of Cardiology at Seoul Asan Medical Center analyzed the valve tissue of a patient with aortic valve stenosis and found that mitochondrial function was reduced and that taking spermidine restored mitochondrial function and inhibited calcification of the aortic valve.



Mitochondria, which supply energy to the cells of our body, exist in our body. It is contained in large quantities in tissues that require a lot of energy, such as the heart and brain. If mitochondrial function is reduced or damaged, it can cause various diseases such as aging, diabetes, cardiovascular disease, and cancer.



Spermidine is a natural substance abundantly contained in natto, cheese, brown rice, mushrooms, broccoli, nuts, and soybeans. It is known to improve mitochondrial function and promote autophagy, which removes unnecessary cells. There has been no report on the role of mitochondria and the effect of spermidine in heart valve tissue.



Professor Lee Sa-min's team first analyzed valve tissue of patients with aortic valve stenosis using an electron microscope and confirmed that mitochondria were damaged compared to normal valve tissue. As a result of quantitative analysis of mitochondrial function using Mitotracker staining, they found that mitochondrial function of patients with aortic valve stenosis was significantly reduced, at about 17%, compared to the normal control group (41%).



In light of this, the research team studied the possibility of treating aortic valve stenosis using spermidine, which is known to improve mitochondrial function.



When the research team administered spermidine to the valve cells of patients with aortic valve stenosis, the expression of genes related to calcification decreased by nearly half. It was confirmed that indicators related to mitochondrial function increased by more than three times.



Furthermore, when an aging mouse animal model was given water containing spermidine, the mitochondrial function of the heart valve tissue improved and the expression of autophagy-related proteins increased. In addition, it showed an effect of suppressing fibrosis and calcification by more than 50% while maintaining the valve thickness at a level similar to that of the normal control group.



This was confirmed through proteome analysis (the entire collection of proteins in the tissue) and additional experimental verification studies that spermidine exerts its effect by reducing DNA methylation due to aging and activating cell metabolism and autophagy to reduce valve calcification.



Professor Lee Sa-min of the Department of Cardiology at Seoul Asan Medical Center said, "We have shown that anti-aging substances such as spermidine can be used as a treatment option for aortic valve stenosis, which has not been treated with drugs until now," and "We plan to further specify the possibility of practical application through future clinical studies."



The results of the study were recently published in the international cardiovascular academic journal, 'Journal of the American College of Cardiology Basic and Translational Medicine (JACC: Basic to Translation Science)'.





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