Modulation of redox-sensitive transcription factors by calorie restriction during aging

Kim, Hyon Jeen; Jung, Kyung Jin; Yu, Byung Pal; Cho, Chong Gun; Choi, Jae Sue; Chung, Hae Young

doi:10.1016/s0047-6374(02)00094-5

Cited by 157 publications

(128 citation statements)

References 34 publications

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“…However, unlike other organs where both MAPK and NF-κB activity increase with age (Kim et al 2002), in lymphocytes, the activation of NF-κB is diminished amongst old subjects (Gupta et al 2005). This is due to age-related alterations in T-cell signalling and CD28 loss, decreasing AKT phosphorylation and DNAbinding activity of the NF-κB complex (reviewed in Larbi et al 2011).…”

Section: Molecular Mediators Of Age-related Inflammationmentioning

confidence: 92%

The role of the T cell in age-related inflammation

Macaulay

Akbar

Henson

2012

AGE

105

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Ageing is accompanied by alterations to T-cell immunity and also by a low-grade chronic inflammatory state termed inflammaging. The significance of these phenomena is highlighted by their being predictors of earlier mortality. We have recently published that the proinflammatory cytokine TNFα is a strong inducer of CD4 + T-cell senescence and T-cell differentiation, adding to the growing body of literature implicating proinflammatory molecules in mediating these critical age-related T-cell alterations. Moreover, the inflammatory process is also being increasingly implicated in the pathogenesis of many common and severe age-related diseases, including cancer, cardiovascular diseases and type 2 diabetes. Furthermore, major age-related risk factors for poor health, such as obesity, stress and smoking, are also associated with an upregulation in systemic inflammatory markers. We propose the idea that the ensuing inflammatory response to influenza infection propagates cardiovascular diseases and constitutes a major cause of influenzarelated mortality. While inflammation is not a negative phenomenon per se, this age-related dysregulation of inflammatory responses may play crucial roles driving age-related pathologies, T-cell immunosenescence and CMV reactivation, thereby underpinning key features of the ageing process.

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Section: Molecular Mediators Of Age-related Inflammationmentioning

confidence: 92%

The role of the T cell in age-related inflammation

Macaulay

Akbar

Henson

2012

AGE

105

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“…Heydari and colleagues reported that CR enhanced the heat shock transcription factor 1 (HSF-1) function and thereby promoted the transcription of the important chaperone, heat shock protein 70 (HSP70) [94] . Kim and coworkers proposed an important role of the following redox-sensitive transcription factors in CR-associated actions including nuclear factor kappa B (NF-κB), activator protein-1 (AP-1); and hypoxia inducible factor-1 (HIF-1) [95] . However, much still remains to be determined with regards to the functioning of transcription factors in long-term CR.…”

Section: Signal Transduction Mechanism Involved In Crmentioning

confidence: 99%

“…Table 1 summaries some of the most important signaling molecules involved in CR-induced biological and physiological responses. FOXO ↓ [89,97] GSK-3β ↓ [93,98] HIF-1 ↓ [95,99] HSF-1 ↑ [94] HSP-70 ↑ [94,100] mTOR ↓ [90,101] NF-κB ↓ [81,82,95,97] PGC-1α ↑ [91,92] PPAR α ↑ [91,102] SIRT1 ↑↓ [92,93,103] ↑=increase in signal transduction; ↓=decrease in signal transduction.…”

Section: Signal Transduction Mechanism Involved In Crmentioning

confidence: 99%

Caloric restriction and heart function: is there a sensible link?

Han

Ren

2010

Acta Pharmacol Sin

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Calorie restriction (CR) is defined as a reduction in calorie intake below the usual ad libitum intake without malnutrition. In general, the daily caloric intake subjected to CR has been restricted to 50% to 70% of the average food intake in subjects eating ad libitum [1,2] . CR was first reported to retard aging and prolong median and maximal life span in the 1930s [3] . Over the last several decades, CR has been widely studied which exhibits an apparent beneficial impact on longevity, ageassociated diseases, and attenuation of functional decline, across a broad variety of species (including rats, mice, fish, flies, worms and yeast) [4,5] . Moreover, CR provides protection against a cadre of chronic diseases including diabetes mellitus, neurodegenerative diseases, autoimmune disorders [6][7][8] and cancer [9][10][11][12] . CR has been shown to alter a variety of physiological parameters especially reduced metabolic rate and oxidative damage, resulting in a decrease in the incidence of cardiovascular diseases [13] . In response to energy deficiency, experimental animals experience a drastic decrease in both fat mass and lean body mass. Muscle mass is overtly reduced, although the rate of loss of function and mass/body weight with the aging process is attenuated [9,[14][15][16] . Metabolic rate may decrease transiently although studies have indicated similar metabolic rate per kg lean body mass to that of ad libitum fed rodents in longterm CR protocol [17] . Body temperature, systolic and diastolic blood pressure all decrease [18,19] along with the reduced sympathetic activity [20] . CR-treated animals are more spontaneously active and display superior cognitive abilities compared to their ad libitum counterparts [21,22] .The most prominent mechanism that may be responsible for the beneficial health and physiological effects of CR are usually mediated through increased insulin sensitivity which results in reduced plasma glucose and insulin concentrations and improved glucose tolerance [23] ; reduced levels of oxidative stress (decreased oxidative damage to proteins, lipids and DNA) [24] , increased resistance to various types of stress including heat, oxidative and metabolic stress [25] as well as enhanced immune function [26] . Impact of CR on agingAn inverse relationship between calorie intake and lifespan has been revealed in mice, suggesting a key role for regulators of energy metabolism in the mechanism of CR. Accordingly, CR-induced metabolic reprogramming may be a key event in the mechanism of lifespan extension [27,28] . The age when CR is started, the severity of restriction, and strain or genetic background of animals determine the magnitude of life extension. The only mammals in which CR has clearly been shown ReviewCaloric restriction and heart function: is there a sensible link? Calorie restriction (CR) is defined as a reduction in calorie intake below the usual ad libitum intake without malnutrition. Ample of clinical and experimental evidence has demonstrated that CR is capable of retarding aging p...

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“…Increasing evidence shows that age-related changes affect the molecular crosstalk between stromal and epithelial cells generating a more permissive environment for tumor development. 1 Cellular senescence is an agerelated process and these cells accumulate in tissues with age. Senescent cells, originally defined in fibroblasts, 2 remained metabolically active but in a growth-arrested state at the G1 phase.…”

mentioning

confidence: 99%

Expression of p14ARF, p15INK4b, p16INK4a, and DCR2 increases during prostate cancer progression

et al. 2006

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Prostate carcinoma is a hormonally driven age-related neoplasm. Cellular senescence is an age-related process where cells remain metabolically active but in a growth-arrested state at the G1 phase. p14 ARF , p15 INK4b , and p16 INK4a , which are known to regulate G1 cell cycle arrest, and the tumor necrosis factor receptor superfamily member decoy receptor 2 (DCR2), have been recently identified as senescence markers. The purpose of this study was to characterize and compare the expression of p14 ARF , p15 INK4b , p16 INK4a , and DCR2 in tissue microarrays containing cases of normal prostate, nodular hyperplasia, prostate intraepithelial neoplasia (PIN), and malignant prostate cancer tissue. We performed immunohistochemical staining for p14 ARF , p15 INK4b , p16 INK4a , and DCR2 in tissue microarray blocks containing 41 cores of normal prostate, 65 cores of nodular hyperplasia, 21 cores of PIN, 69 cores of low-grade prostate carcinoma, and 42 cores of high-grade prostate carcinoma, derived from 80 cases of prostatectomy with adenocarcinomas. We detected positive staining of p16 INK4a in 19% of the PIN, 25% of the low-grade carcinoma, and 43% of the high-grade carcinoma specimens but none in the normal prostate and nodular hyperplasia specimens. Expression of p14 ARF revealed very high levels of expression in normal tissues (83%), nodular hyperplasia (88%), PIN (89%), and cancer cells (100%). P15 INK4b and DCR2 were found positive in 81 and 33% normal, 46 and 10% nodular hyperplasia, 74 and 36% PIN tissues, 87 and 89% low-grade carcinomas, and 100 and 93% high-grade carcinomas. There is an increased protein expression of senescence-associated molecular markers, indicating that cellular senescence might play a role in prostate carcinoma. Because p16 INK4a -positive cells were detected only in premalignant lesions and carcinomas but not in normal or benign tissues, p16 INK4a may aid in the diagnosis of PIN and prostate cancer in difficult cases.

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Modulation of redox-sensitive transcription factors by calorie restriction during aging

Cited by 157 publications

References 34 publications

The role of the T cell in age-related inflammation

The role of the T cell in age-related inflammation

Caloric restriction and heart function: is there a sensible link?

Expression of p14ARF, p15INK4b, p16INK4a, and DCR2 increases during prostate cancer progression

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