We revealed some features of the neurohumoral and immune profile in preschool children with functional disorders of the autonomic nervous system (ANS) associated with the polymorphism of the SIRT1 gene (rs7069102) responsible for stability of the cell cycle, energy and plastic metabolism of organic substances, and Ca2+ exchange. The neurohumoral profile of the surveyed children is characterized by excessive content of glutamic acid and serotonin, which leads to excessive synaptic activation and disorders of ANS inhibition (p<0.05). The cell immune profile is characterized by a reduced immunoregulatory index CD4+/CD8+ with a simultaneous deficiency of CD3+CD4+ and excess of CD3+CD8+ lymphocytes (p<0.05). These etiopathogenetic disorders of the neurohumoral and immune profile are associated with variant G-allele of the SIRT1 gene (rs7069102) and the corresponding homozygous GG-genotype (p<0.05), which leads to disturbances in the control of the cell cycle stability, including apoptosis, cytochrome deacetylation, inhibition of the glutamate dehydrogenase enzyme activity with excessive glutamate accumulation, energy metabolism in mitochondria, and Ca2+ exchange. The revealed features of neurotransmitters content (excess of serotonin and glutamic acid) and indicators of cell immunity (reduced proportion of CD4+/CD8+ cells) associated with the variant G allele and GG genotype of the SIRT1 gene (rs7069102) form a complex of neurohumoral, immune, and genetic markers in children with functional disorders of ANS (G90.8). This allows recommending them as indicators for early diagnosis and prevention of autonomic disorders in children.
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Translated from Byulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 172, No. 11, pp. 622-626, November, 2021
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Dolgikh, О.V., Zaitseva, N.V. & Nikonoshina, N.A. Features Neurohumoral and Immune Profile in Children with Functional Disorders of the Autonomic Nervous System Associated with Sirtuin Gene SIRT1 (rs7069102) Polymorphism. Bull Exp Biol Med 172, 583–586 (2022). https://doi.org/10.1007/s10517-022-05439-w
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DOI: https://doi.org/10.1007/s10517-022-05439-w