Selenot, also known as Selenoprotein T (SELENOT), is a thioredoxin-like enzyme anchored at the endoplasmic reticulum (ER) membrane. It is highly conserved evolutionarily and plays a crucial role in maintaining ER proteostasis, endocrine homeostasis, and neuroprotection. SELENOT is involved in redox regulation, and its deficiency can lead to various cellular dysfunctions. Gene knockout models, especially in mice, have been instrumental in studying its functions [4,5].

In mouse models, brain-specific SELENOT knockout led to a significant decrease in the number of tyrosine hydroxylase-positive catecholaminergic neurons in specific brain areas, indicating its importance in the establishment of the catecholaminergic neuronal system [1]. Also, in female rats with facial nerve injury, a mimetic peptide PSELT derived from SELENOT promoted nerve regeneration by increasing axonal myelination [2]. In the context of heart failure, PSELT attenuated systemic inflammation, myocardial injury, and improved cardiac contractile function in aged spontaneously hypertensive heart failure rats [3].

In conclusion, SELENOT is essential for normal development, endocrine function, and neural and cardiac health. Mouse knockout models have revealed its role in maintaining the density of catecholaminergic neurons, promoting nerve regeneration, and protecting against heart failure, providing insights into potential therapeutic strategies for related diseases.