The Impact of Selenium Deficiency on Cardiovascular Function

Abstract

Selenium (Se) is an essential trace element that is necessary for various metabolic processes, including protection against oxidative stress, and proper cardiovascular function. The role of Se in cardiovascular health is generally agreed upon to be essential yet not much has been defined in terms of specific functions. Se deficiency was first associated with Keshan's Disease, an endemic disease characterized by cardiomyopathy and heart failure. Since then, Se deficiency has been associated with multiple cardiovascular diseases, including myocardial infarction, heart failure, coronary heart disease, and atherosclerosis. Se, through its incorporation into selenoproteins, is vital to maintain optimal cardiovascular health, as selenoproteins are involved in numerous crucial processes, including oxidative stress, redox regulation, thyroid hormone metabolism, and calcium flux, and inadequate Se may disrupt these processes. The present review aims to highlight the importance of Se in cardiovascular health, provide updated information on specific selenoproteins that are prominent for proper cardiovascular function, including how these proteins interact with microRNAs, and discuss the possibility of Se as a potential complemental therapy for prevention or treatment of cardiovascular disease.

Keywords: Keshan’s Disease; cardiovascular; heart; selenium; selenoproteins.

Figure 1

Potential mechanism of how Se deficiency impacts Se metabolism and contributes to cardiovascular diseases. Se acquired through the diet can go through the trans-selenation pathway and be directly converted to Sec, becoming hydrogen selenide. In cases of low Se, stress-responsive selenoprotein synthesis may be affected. Those selenoproteins with known function in the heart are shown above but it is still unknown how some of these proteins contribute to the development of cardiovascular disease in cases of Se deficiency. Decreased levels of Se may negatively impact redox regulation, thyroid hormone metabolism, and calcium flux while increasing atherogenesis and oxidative stress. This, in turn, may lead to several cardiovascular diseases, including heart failure, myocardial infarction, cardiomyopathy, and atherosclerosis. Red arrows indicate processes and proteins that are decreased while green arrows indicate processes that are increased during Se deficiency. Black arrows point to known relationships, and dashed gray lines indicate the relationships that have not been established yet in the heart. The “?” indicates mechanisms that have not been determined. Se, selenium; Sec, selenocysteine; HSe–, hydrogen selenide; SEPHS2, selenophosphate synthetase 2; GPX, glutathione peroxidase; TXNRDs, thioredoxin reductases; DIO, iodothyronine deiodinases; SELENOP, selenoprotein P; SELENOT, selenoprotein T; SELENOK, selenoprotein K; MSRB1, methionine sulfoxide reductase B1; SELENOW, selenoprotein W. Heart was used from Servier Medical Art (smart.servier.com).