Publications by authors named "N A Kurochkina"

Article Synopsis
  • The study explored how knocking out six Hsp70 genes affects gene expression related to aging in the leg muscles of Drosophila melanogaster (fruit flies).
  • Researchers compared the transcriptomic profiles of control flies (w^(1118)) with those of Hsp70^(-) flies at various ages (7, 23, and 47 days).
  • Findings revealed that Hsp70^(-) flies had a shorter lifespan and lower locomotion speed, alongside significant changes in muscle transcriptome and energy metabolism enzyme levels, suggesting a possible compensatory mechanism involving other chaperone genes.
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The functions of the heat shock protein 70 () genes were studied using a line of with a knockout of 6 of these genes out of 13. Namely, the effect of knockout of genes on negative geotaxis climbing (locomotor) speed and the ability to adapt to climbing training (0.5-1.

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A decrease in muscle mass and its functionality (strength, endurance, and insulin sensitivity) is one of the integral signs of aging. One of the triggers of aging is an increase in the production of mitochondrial reactive oxygen species. Our study was the first to examine age-dependent changes in the production of mitochondrial reactive oxygen species related to a decrease in the proportion of mitochondria-associated hexokinase-2 in human skeletal muscle.

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Evaluation of the influence of primary and secondary aging on the manifestation of molecular and cellular hallmarks of aging is a challenging and currently unresolved issue. Our study represents the first demonstration of the distinct role of primary aging and chronic inflammation/physical inactivity - the most important drivers of secondary aging, in the regulation of transcriptomic and proteomic profiles in human skeletal muscle. To achieve this purpose, young healthy people (n = 15), young (n = 8) and older (n = 37) patients with knee/hip osteoarthritis, a model to study the effect of long-term inactivity and chronic inflammation on the vastus lateralis muscle, were included in the study.

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Inherited painless neuropathies arise due to genetic insults that either block the normal signaling of or destroy the sensory afferent neurons in the dorsal root ganglion (DRG) responsible for transducing noxious stimuli. Complete loss of these neurons leads to profound insensitivity to all sensory modalities including pain. Hereditary sensory and autonomic neuropathy type 2 (HSNAII) is a rare genetic neuropathy characterized by a progressive distal early onset sensory loss.

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