Influence of aging and calorie restriction on MAPKs activity in rat kidney

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

doi:10.1016/s0531-5565(02)00082-7

Cited by 71 publications

(42 citation statements)

References 69 publications

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“…5); H 2 O 2 may act at multiple levels to activate JNK (and p38): dissociation of thioredoxin from the ASK-1 complex (204), disruption of the glutathione transferase (GT)-JNK complex (1), or inhibition of MAPK phosphatase activity (76). Basal JNK activity, but not its protein levels, is increased in mouse brain and liver, rat kidney and splenic lymphocytes, and human skeletal muscle during aging (105,127,142,221,242). Basal activities of ERK and p38 kinase, but not their protein levels, are reported to decrease in the brain cortex during aging, a phenomenon that was prevented by caloric restriction (259); conversely, basal p38 and ERK activities were increased in mouse liver, rat kidney, and human skeletal muscle (104,127,242).…”

Section: Mitochondrial Regulation Of Cytosolic Signalingmentioning

confidence: 99%

“…Basal JNK activity, but not its protein levels, is increased in mouse brain and liver, rat kidney and splenic lymphocytes, and human skeletal muscle during aging (105,127,142,221,242). Basal activities of ERK and p38 kinase, but not their protein levels, are reported to decrease in the brain cortex during aging, a phenomenon that was prevented by caloric restriction (259); conversely, basal p38 and ERK activities were increased in mouse liver, rat kidney, and human skeletal muscle (104,127,242). It is unclear whether or not these discrepancies are due to tissue specificity of p38 and ERK responses to the aging process.…”

Section: Mitochondrial Regulation Of Cytosolic Signalingmentioning

confidence: 99%

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Mitochondrial Energy Metabolism and Redox Signaling in Brain Aging and Neurodegeneration

Yin

Boveris²,

Cadenas³

2014

Antioxidants & Redox Signaling

214

166

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Significance: The mitochondrial energy-transducing capacity is essential for the maintenance of neuronal function, and the impairment of energy metabolism and redox homeostasis is a hallmark of brain aging, which is particularly accentuated in the early stages of neurodegenerative diseases. Recent Advances: The communications between mitochondria and the rest of the cell by energy-and redox-sensitive signaling establish a master regulatory device that controls cellular energy levels and the redox environment. Impairment of this regulatory devise is critical for aging and the early stages of neurodegenerative diseases. Critical Issues: This review focuses on a coordinated metabolic network-cytosolic signaling, transcriptional regulation, and mitochondrial function-that controls the cellular energy levels and redox status as well as factors which impair this metabolic network during brain aging and neurodegeneration. Future Directions: Characterization of mitochondrial function and mitochondria-cytosol communications will provide pivotal opportunities for identifying targets and developing new strategies aimed at restoring the mitochondrial energy-redox axis that is compromised in brain aging and neurodegeneration. Antioxid. Redox Signal. 20, 353-371.

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Section: Mitochondrial Regulation Of Cytosolic Signalingmentioning

confidence: 99%

Section: Mitochondrial Regulation Of Cytosolic Signalingmentioning

confidence: 99%

Mitochondrial Energy Metabolism and Redox Signaling in Brain Aging and Neurodegeneration

Yin

Boveris²,

Cadenas³

2014

Antioxidants & Redox Signaling

214

166

View full text Add to dashboard Cite

show abstract

“…We therefore chose to select endothelial cell type YPEN-1 cell line. Recent publications from our laboratory presented evidence that NF-κ B activation increases during the aging process in kidney homogenate of rat and YPEN-1 cell (Chung et al ., 2002;Go et al ., 2005).…”

Section: Introductionmentioning

confidence: 98%

Modulation of the age‐related nuclear factor‐κB (NF‐κB) pathway by hesperetin

et al. 2006

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SummaryNuclear factor-κ κ κ κ B (NF-κ κ κ κ B), a redox-sensitive transcription factor, plays an important role in the aging process. Thus, developing and identifying specific components that modulate NF-κ κ κ κ B without adverse side-effects would be of major importance. Hesperetin, a flavanone abundant in citrus fruits, has a variety of pharmacological properties being antioxidant, cholesterol-lowering, and antiinflammatory.In this study, we investigated how hesperetin fed to 6-and 24-month-old rats modulates NF-κ κ κ κ B in their kidneys. Results showed that hesperetin suppressed NF-κ κ κ κ B activation and related gene expressions. An even more interesting finding is that hesperetin suppressed NF-κ κ κ κ B through four signal transduction pathways, NIK/IKK, ERK, p38, and JNK. Further evidence showed the remarkable efficacy of hesperetin to suppress the translocation of Trx/Ref-1, indicating its beneficial effect on the redox status. The most significant findings of the current study report new information on the use of hesperetin as a potential anti-aging agent.

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“…Mammalian cells, with the exceptions of germ line cells and stem cells, have a limited replication potential in vivo, defined as replicative senescence, which amounts to irreversible growth arrest after a limited number of cell divisions [19]. Cellular senescence is also associated with reactive oxygen species (ROS), the incessant damaging products generated from aerobic metabolism such as oxidative stress [20][21][22][23]. During the pathogenesis of type 2 diabetes, beta cell proliferation increases to compensate for the increased insulin demand caused by insulin resistance, and the generation of ROS is induced by hyperglycaemia [6-8, 12, 24].…”

Section: Introductionmentioning

confidence: 99%

Pancreatic beta cell senescence contributes to the pathogenesis of type 2 diabetes in high-fat diet-induced diabetic mice

2004

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Aims/hypothesis: During the pathogenesis of type 2 diabetes insulin resistance causes compensatory proliferation of beta cells. As beta cells have a limited replication potential, this compensatory proliferation might accelerate cellular senescence and lead to diabetes. We examined the cellular senescence of beta cells after proliferation during lipoglucotoxicity. Methods: Senescence-associated markers in beta cells were examined in nutrient-induced diabetic C57BL/6J mice that were fed a high-fat diet. After 4 and 12 months of the high-fat diet, intraperitoneal glucose tolerance tests (IPGTTs) and histochemical analyses of Ki-67, p38, senescence-associated beta-galactosidase, and beta cell mass were performed. Results: At 4 months, the AUC for plasma insulin levels during the IPGTT (AUC insulin ) was higher, beta cell mass was 3.1-fold greater, and the proliferation of beta cells was 2.2-fold higher than in the control group. However, at 12 months, AUC insulin declined, the frequency of Ki-67-positive beta cells decreased to one-third that of the control group, and the senescence-associated, beta-galactosidasepositive area increased to 4.7-fold that of the control group. Moreover, small amounts of p38, which is induced by oxidative stress and mediates cellular senescence, were found in beta cells from the high-fat diet group, but not in beta cells from the control group. Furthermore, the senescence-associated, beta-galactosidase-positive area in the high-fat diet group had a highly significant negative correlation with AUC insulin (r=−0.852, p<0.01). Conclusions/interpretation: Beta cell senescence occurred in diet-induced type 2 diabetes and led to insufficient insulin release. These findings suggest that cellular senescence contributes to the pathogenesis of diet-induced diabetes.

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Influence of aging and calorie restriction on MAPKs activity in rat kidney

Cited by 71 publications

References 69 publications

Mitochondrial Energy Metabolism and Redox Signaling in Brain Aging and Neurodegeneration

Mitochondrial Energy Metabolism and Redox Signaling in Brain Aging and Neurodegeneration

Modulation of the age‐related nuclear factor‐κB (NF‐κB) pathway by hesperetin

Pancreatic beta cell senescence contributes to the pathogenesis of type 2 diabetes in high-fat diet-induced diabetic mice

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