What Do We Know About Selenium Contributions to Muscle Physiology?

Abstract

Early observations of selenium (Se) deficiencies in human and livestock revealed the importance of this trace element for normal muscle function. However, the molecular and cellular mechanisms impaired consecutive to low Se diet and its connection to the muscular diseases remain elusive. Importantly, mutations in the SEPN1 gene encoding selenoprotein N (SEPN1) were shown to cause an inherited muscular disease in humans.Therefore, it is expected that understanding the role of SEPN1 and the related pathophysiology will unveil the participation of Se in molecular processes essential for muscle function and pave the way for targeted therapeutics. However, the functional characterization of SEPN1 is still lacking. Analysis of its activity in cellular and animal models pointed to its involvement in oxidative stress defense and in control of calcium (Ca 2+ ) handling. A link between the activities of SEPN1 and of the Ca 2+ transporters RyR1 and SERCA was shown, but the enzymatic reaction catalyzed by SEPN1 has not been characterized.

Uncovering the Importance of Selenium in Muscle Disease

“…Both zebrafish and mouse animal models were designed to decipher the underlying molecular and physiological dysfunctions arising from SELENON gene mutations. The data collected from these models addressing the role of SELENON activity in muscle development and maintenance, as well as during muscle regeneration, were reviewed elsewhere (Castets et al 2012;Lescure et al 2016). Here we are focusing on the analysis and combination of information resulting from studies of in vitro, ex vivo and in vivo models.…”