The paradoxical role of thioredoxin on oxidative stress and aging

Cunningham, Geneva M.; Roman, Madeline G.; Flores, Lisa C.; Hubbard, Gene B.; Salmon, Adam B.; Zhang, Yiqiang; Gelfond, Jonathan; Ikeno, Yuji

doi:10.1016/j.abb.2015.02.025

Cited by 53 publications

(32 citation statements)

References 87 publications

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“…Down regulation of TRX in mice showed no beneficial effect on lifespan. However, these studies demonstrate that reduced levels of TRX may be more important for tumor development than aging . Since, TRX levels remain constant during life we speculated that the activity of TRX is regulated by its natural inhibitor TXNIP during aging.…”

mentioning

confidence: 99%

Enhanced expression of thioredoxin‐interacting‐protein regulates oxidative DNA damage and aging

et al. 2018

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The “free radical theory of aging” suggests that reactive oxygen species (ROS) are responsible for age‐related loss of cellular functions and, therefore, represent the main cause of aging. Redox regulation by thioredoxin‐1 (TRX) plays a crucial role in responses to oxidative stress. We show that thioredoxin‐interacting protein (TXNIP), a negative regulator of TRX, plays a major role in maintaining the redox status and, thereby, influences aging processes. This role of TXNIP is conserved from flies to humans. Age‐dependent upregulation of TXNIP results in decreased stress resistance to oxidative challenge in primary human cells and in Drosophila. Experimental overexpression of TXNIP in flies shortens lifespan due to elevated oxidative DNA damage, whereas downregulation of TXNIP enhances oxidative stress resistance and extends lifespan.

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mentioning

confidence: 99%

Enhanced expression of thioredoxin‐interacting‐protein regulates oxidative DNA damage and aging

et al. 2018

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“…However, a conflicting report from the same group recently stated that the Trx1 +/− mutation failed to increase life span. Preliminary results also indicated that the Trx1 and Trx2 double heterozygous deletion increases life span while still sensitizing these animals to oxidative stress (111). During the last decade, it has been demonstrated in C. elegans and mice that slight amounts of oxidative stress due to specific disruption of mitochondrial ETC or by direct treatment of animals with H 2 O 2 can result in a hormetic effect, producing upregulation of stress-response pathways and ultimately increased life span (112).…”

Section: Role Of Oxidative Stress In Agingmentioning

confidence: 92%

Signaling Networks Determining Life Span

Riera

Merkwirth

Filho

et al. 2016

Annu. Rev. Biochem.

148

129

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The health of an organism is orchestrated by a multitude of molecular and biochemical networks responsible for ensuring homeostasis within cells and tissues. However, upon aging, a progressive failure in the maintenance of this homeostatic balance occurs in response to a variety of endogenous and environmental stresses, allowing the accumulation of damage, the physiological decline of individual tissues, and susceptibility to diseases. What are the molecular and cellular signaling events that control the aging process and how can this knowledge help design therapeutic strategies to combat age-associated diseases? Here we provide a comprehensive overview of the evolutionarily conserved biological processes that alter the rate of aging and discuss their link to disease prevention and the extension of healthy life span.

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“…However, high and moderately elevated levels of H 2 S have also been shown to inhibit cytochrome c oxidase, react with other heme- and sulfur-containing proteins and contribute to disease thus, the amount of this gasotransmitter is likely tightly controlled and needs further study (Ueki et al, 2011; Roman et al, 2013; Dorman et al, 2002; Goubern et al, 2007). Moreover, enhanced resistance to oxidative stress is only one piece of the puzzle in terms of lifespan extension (Perez et al, 2009; Dai et al, 2014; Cunningham et al, 2015; Speakman et al, 2015). Methionine restriction may itself directly activate NRF2.…”

Section: 4 Methionine Catabolism: the Transsulfuration Pathwaymentioning

confidence: 99%

Cutting back on the essentials: Can manipulating intake of specific amino acids modulate health and lifespan?

Brown‐Borg

Buffenstein

2017

Ageing Research Reviews

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With few exceptions, nutritional and dietary interventions generally impact upon both old-age quality of life and longevity. The life prolonging effects, commonly observed with dietary restriction reportedly are linked to alterations in protein intake and specifically limiting the dietary intake of certain essential amino acids. There is however a paucity of data methodically evaluating the various essential amino acids on health- and lifespan and the mechanisms involved. Rodent diets containing either lower methionine content, or tryptophan, than that found in commercially available chow, appear to elicit beneficial effects. It is unclear whether all of these favorable effects associated with restricted intake of methionine and tryptophan are due to their specific unique properties or if restriction of other essential amino acids, or proteins in general, may produce similar results. Considerably more work remains to be done to elucidate the mechanisms by which limiting these vital molecules may delay the onset of age-associated diseases and improve quality of life at older ages.

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The paradoxical role of thioredoxin on oxidative stress and aging

Cited by 53 publications

References 87 publications

Enhanced expression of thioredoxin‐interacting‐protein regulates oxidative DNA damage and aging

Enhanced expression of thioredoxin‐interacting‐protein regulates oxidative DNA damage and aging

Signaling Networks Determining Life Span

Cutting back on the essentials: Can manipulating intake of specific amino acids modulate health and lifespan?

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