2010
DOI: 10.1089/ars.2009.3074
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Cellular Stress Responses, The Hormesis Paradigm, and Vitagenes: Novel Targets for Therapeutic Intervention in Neurodegenerative Disorders

Abstract: Despite the capacity of chaperones and other homeostatic components to restore folding equilibrium, cells appear poorly adapted for chronic oxidative stress that increases in cancer and in metabolic and neurodegenerative diseases. Modulation of endogenous cellular defense mechanisms represents an innovative approach to therapeutic intervention in diseases causing chronic tissue damage, such as in neurodegeneration. This article introduces the concept of hormesis and its applications to the field of neuroprotec… Show more

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Cited by 716 publications
(615 citation statements)
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References 479 publications
(635 reference statements)
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“…This finding is consistent with evidence suggesting that the HO-1 gene is redox regulated and, similar to other antioxidant enzymes [50], this occurs because it contains in its promoter region the antioxidant responsive element (ARE). Therefore, the HO-1 gene undergoes a redox sensitive modulation by transcription factors recognizing specific binding sites within the promoter and distal enhancer regions of the HO-1 gene [14,15]. In addition, heme oxygenase-1 is rapidly upregulated by oxidative and nitrosative stresses, as well as by glutathione depletion [51].…”
Section: Discussionmentioning
confidence: 99%
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“…This finding is consistent with evidence suggesting that the HO-1 gene is redox regulated and, similar to other antioxidant enzymes [50], this occurs because it contains in its promoter region the antioxidant responsive element (ARE). Therefore, the HO-1 gene undergoes a redox sensitive modulation by transcription factors recognizing specific binding sites within the promoter and distal enhancer regions of the HO-1 gene [14,15]. In addition, heme oxygenase-1 is rapidly upregulated by oxidative and nitrosative stresses, as well as by glutathione depletion [51].…”
Section: Discussionmentioning
confidence: 99%
“…Despite the abundance and apparent capacity of chaperones and other components of homeostasis to restore folding equilibrium, brain cells appears poorly adapted for chronic proteotoxic stress which increases in neurodegenerative diseases such as MS [14]. In these conditions, a decline in biosynthetic and repair activities that compromises the integrity of the proteome is strongly influenced by protective genes called ''vitagenes'' that control aging, thus linking stress and protein homeostasis with the health antidegenerative mechanisms [15]. Vitagenes encode for heat shock proteins (Hsp) Hsp32, Hsp70, the thioredoxin and the sirtuin protein systems.…”
Section: Introductionmentioning
confidence: 99%
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“…CR, a robust anti‐aging intervention that extends lifespan in almost all organisms tested, is accompanied by the rescue of age‐associated decline of CYB5R3 and NQO1 function [reviewed in (de Cabo, Siendones, Minor & Navas, 2009; Hyun, Hernandez, Mattson & de Cabo, 2006)]. Likewise, several pharmacological and genetical‐based strategies targeting these enzymes have been employed to ultimately delay aging and age‐related metabolic diseases (Calabrese, Cornelius, Dinkova‐Kostova, Calabrese & Mattson, 2010; Lee et al., 2012; Martin‐Montalvo et al., 2016; Rizvi & Pandey, 2010; Varela‐Lopez, Giampieri, Battino & Quiles, 2016). CYB5R3 catalyzes a two‐step one‐electron transfer reaction in which NADH is oxidized and coenzyme Q (CoQ) is reduced.…”
Section: Introductionmentioning
confidence: 99%