Purpose of review: (Mal-)nutrition of micronutrients, like selenium, has great impact on the human heart and improper micronutrient intake was observed in 30-50% of patients with heart failure. Low selenium levels have been reported in Europe and Asia and thought to be causal for Keshan disease. Selenium is an essential micronutrient that is needed for enzymatic activity of the 25 so-called selenoproteins, which have a broad range of activities. In this review, we aim to summarize the current evidence about selenium in heart failure and to provide insights about the potential mechanisms that can be modulated by selenoproteins.
Recent findings: Suboptimal selenium levels (<100 μg/L) are prevalent in more than 70% of patients with heart failure and were associated with lower exercise capacity, lower quality of life, and worse prognosis. Small clinical trials assessing selenium supplementation in patients with HF showed improvement of clinical symptoms (NYHA class), left ventricular ejection fraction, and lipid profile, while governmental interventional programs in endemic areas have significantly decreased the incidence of Keshan disease. In addition, several selenoproteins are found impaired in suboptimal selenium conditions, potentially aggravating underlying mechanisms like oxidative stress, inflammation, and thyroid hormone insufficiency. While the current evidence is not sufficient to advocate selenium supplementation in patients with heart failure, there is a clear need for high level evidence to show whether treatment with selenium has a place in the contemporary treatment of patients with HF to improve meaningful clinical endpoints. Graphical summary summarizing the potential beneficial effects of the various selenoproteins, locally in cardiac tissues and systemically in the rest of the body. In short, several selenoproteins contribute in protecting the integrity of the mitochondria. By doing so, they contribute indirectly to reducing the oxidative stress as well as improving the functionality of immune cells, which are in particular vulnerable to oxidative stress. Several other selenoproteins are directly involved in antioxidative pathways, next to excreting anti-inflammatory effects. Similarly, some selenoproteins are located in the endoplasmic reticulum, playing roles in protein folding. With exception of the protection of the mitochondria and the reduction of oxidative stress, other effects are not yet investigated in cardiac tissues. The systemic effects of selenoproteins might not be limited to these mechanisms, but also may include modulation of endothelial function, protection skeletal muscles, in addition to thyroid metabolism.
Abbreviations: DIO, iodothyronine deiodinase; GPx, glutathione peroxidase; MsrB2, methionine-R-sulfoxide reductase B2; SELENOK, selenoprotein K; SELENON, selenoprotein N; SELENOP, selenoprotein P; SELENOS, selenoprotein S; SELENOT, selenoprotein T; TXNRD, thioredoxin reductase.
Keywords: Heart failure; Selenium; Selenoproteins.