A new cause underlying the formation of thoracic aortic aneurysms has been identified. This was identified by international research involving the State University of Milan and the Irccs Italian Auxological Institute published in 'Nature Communications': it is a deficiency of specific selenoproteins (SeP), caused by a hereditary defect, which leads to accumulation of oxidative stress. The study was conducted on data collected both on humans and on mouse and zebrafish models.
SePs – a note details – are a family of proteins that include a rare selenium-containing amino acid, selenocysteine. Most of them are involved in protecting the body against oxidative stress, reducing the levels of 'reactive oxygen species' (Ros) and lipid peroxidation. A characteristic biochemical signature of the circulating levels of the hormones T3 (low) and T4 (high) led to the identification a few years ago of a rare genetic defect affecting the SecisBP2 gene, which encodes a protein responsible for the insertion of selenocystenins into the inside the SeP.
“These studies indicate a key role for oxidative stress and cell death, through the ferroptosis mechanism, in mediating the degeneration of the aortic walls. Furthermore, the data we collected in zebrafish indicate how an anti-oxidant treatment with α-tocopherol o MitoQ can prevent this particular aortopathy and the related lethality” comment the authors Federica Marelli, researcher at Auxologico, and Luca Persani, endocrinologist professor at the State University of Milan and Auxologico.
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