Browsing by Subject "stress activated protein kinase"

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    Insulin resistance is an evolutionarily conserved physiological mechanism at the cellular level for protection against increased oxidative stress
    (2007) Erol A.
    Several protective cellular mechanisms protect against the accumulation of reactive oxygen species (ROS) and the concomitant oxidative stress. Therefore, any reduction in glucose or fatty acid flux into cells leading to a decrease in the production of reducing equivalents would also lead to a decreased ROS production and protect cells against oxidative stress. In the presence of insulin, FOXO proteins are localized from the nucleus to the cytoplasm and degraded. An increase in cellular glucose uptake will lead to increased production of ROS. This in turn activates the stress-responsive Jun-N-terminal kinase (JNK), which promotes nuclear translocation of FOXO proteins, upregulating some important target genes including stress resistance. Consequently, insulin resistance should result in decreased cellular ROS production. For this reason, insulin resistance could be a physiological mechanism activated at the cellular level in response to conditions stimulating ROS production and leading to the prevention of oxidative stress, and extension of life. Concerning the whole organism, however, IR is a maladaptive process in the long term causing a diabetic state. © 2007 Wiley Periodicals, Inc.
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    JNK/FOXO may be key mechanistic pathway for the hormetic anti-aging
    (2007) Erol A.
    FOXO transcription factors and evolutionarily conserved c-jun N-terminal kinase (JNK) could hold the key to counteract hormetic anti-aging and common diseases. Hormesis is increasingly recognized as a mechanism underlying the beneficial anti-aging effects of certain genetic and environmental factors. Caloric restriction and exercise increase the resistance of organisms to stress and activate stress resistance pathways in cells in different tissues throughout the body by hormesis based mechanism. JNK triggers the relocalization of FOXO factors to the nucleus inducing the expression of FOXO dependent stress response and damage repairing genes. This adaptive response to stress stimuli may play an important role in regulating homeostasis at the organismal level and contribute to longevity.