Up‐regulation of plasma membrane‐associated redox activities in neuronal cells lacking functional mitochondria

Hyun, Dong Hoon; Hunt, Nicole; Emerson, Scott S.; Hernandez, Joe O.; Mattson, Mark P.; Cabo, Rafael de

doi:10.1111/j.1471-4159.2006.04411.x

Cited by 61 publications

(48 citation statements)

References 68 publications

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“…67 This function is driven in cooperation with mitochondria, an interaction particularly observed in °cells. 48,68,69 The ratio of pyridine nucleotides is considered an important regulator of yeast lifespan, as well as the establishment of respiration. 70 The ratio of NAD ϩ /NADH is also an important regulator of the deacetylase activity of Sir2, an enzyme involved in the regulation of lifespan in yeast.…”

Section: Cr Increases Coenzyme Q-dependent Reductases In Plasma Membrmentioning

confidence: 99%

Mechanisms Underlying Caloric Restriction and Lifespan Regulation

Ungvári

Parrado-Fernández

Csiszár

et al. 2008

Circulation Research

212

189

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Abstract-This review focuses on the emerging evidence that attenuation of the production of reactive oxygen species and inhibition of inflammatory pathways play a central role in the antiaging cardiovascular effects of caloric restriction. Particular emphasis is placed on the potential role of the plasma membrane redox system in caloric restriction-induced pathways responsible for sensing oxidative stress and increasing cellular oxidative stress resistance. We propose that caloric restriction increases bioavailability of NO, decreases vascular reactive oxygen species generation, activates the Nrf2/antioxidant response element pathway, inducing reactive oxygen species detoxification systems, exerts antiinflammatory effects, and, thereby, suppresses initiation/progression of vascular disease that accompany aging. (Circ Res. 2008;102:519-528.)

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Section: Cr Increases Coenzyme Q-dependent Reductases In Plasma Membrmentioning

confidence: 99%

Mechanisms Underlying Caloric Restriction and Lifespan Regulation

Ungvári

Parrado-Fernández

Csiszár

et al. 2008

Circulation Research

212

189

View full text Add to dashboard Cite

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“…The cytotoxic actions of H 2 O 2 are complicated, and perhaps mediated, in part, through mitochondria [2,[5][6][7][8]. As a source of reactive oxygen species (ROS) and a sensor of oxidative stress [9,10], mitochondria play a key role in regulation of apoptosis under a variety of pathological conditions, including ischemia, hypoxia, and myocardial infarction [11][12][13][14].…”

Section: Introductionmentioning

confidence: 99%

Insulin-like growth factor-1 receptor activation prevents hydrogen peroxide-induced oxidative stress, mitochondrial dysfunction and apoptosis

Hao

Geng

et al. 2011

Apoptosis

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Vascular disease is the leading cause of morbidity and mortality. Oxidative stress can cause endothelial cell apoptosis. Low insulin like growth factor-1 (IGF-1) has been linked to adverse risk profile and increased vascular disease incidence. Since IGF-1 acts as an important survival factor for multiple cell types, we undertook this study to investigate whether IGF-1 favorably affects oxidative-stress mediated apoptosis of vascular endothelial cells. Exposure to hydrogen peroxide induced apoptotic changes (e.g. DNA fragmentation, altered mitochondrial membrane potential and caspase-3 activity) in human umbilical vein endothelial cells (HUVECs) in a time dependent manner. Addition of IGF-1 blocked the oxidative-stress effect parallel to IGF-1 receptor (IGF-1R) expression, and silencing the IGF-1R with small interference RNA attenuated the IGF-1 influence. Our findings show that enhanced IGF-1 signaling inhibits oxidative-stress induced apoptosis in HUVECs by reducing mitochondrial dysfunction. Specifically the protective mechanism of IGF-1 involves preserving the mitochondrial membrane potential, maintaining the mitochondrial retention of cytochrome-c, and reducing caspase-3 activity. These results may have therapeutic implications in preventing/reducing vascular disease associated endothelial dysfunction.

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“…(179)(180)(181) The upregulation of plasma membrane redox system that occurs during CR decreases the levels of oxidative stress in aged membranes. (182)(183)(184)(185) CR modifies composition of fatty acid in plasma membrane, resulting in decreased oxidative damage including lipid peroxidation. (186,187) More importantly, plasma membrane redox activities and also the content of CoQ, which decline with age, are enhanced by CR, providing protection to phospholipids and preventing lipid peroxidation reaction progression.…”

Section: Sirtuin Class O Of Forkhead Box Transcription Factors (Foxomentioning

confidence: 99%

“…(186,187) More importantly, plasma membrane redox activities and also the content of CoQ, which decline with age, are enhanced by CR, providing protection to phospholipids and preventing lipid peroxidation reaction progression. (182)(183)(184)(185) The logical extension of this idea is that it should be possible to mimic the beneficial effects of dieting and exercise by tweaking the right pathways, using small molecules. Studies with "CR mimetics" such as resveratrol and metformin (which activate the SIRT1-AMPK system) or rapamycin (which inhibits mTOR), show that it is possible for a rodent to be obese and sedentary while maintaining the physiology of a lean animal.…”

Section: Sirtuin Class O Of Forkhead Box Transcription Factors (Foxomentioning

confidence: 99%

Molecular Mechanisms of Cardiovascular Aging

Meiliana

Wijaya

2013

Indones Biomed J

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BACKGROUND: The average lifespan of humans is increasing, and with it the percentage of people entering the 65 and older age group is growing rapidly and will continue to do so in the next 20 years. Within this age group, cardiovascular disease will remain the leading cause of death, and the cost associated with treatment will continue to increase. Aging is an inevitable part of life and unfortunately poses the largest risk factor for cardiovascular disease.CONTENT: We provide an overview of some of the molecular mechanisms involved in regulating lifespan and health, including mitochondria, telomeres, stem cells, sirtuins, Adenosine Monophosphate-activated Protein Kinase, Mammalian Target of Rapamycin and Insulin-like Growth Factor 1. We also provide future perspectives of lifespan and health, which are intimately linked fields.SUMMARY: Aging remains the biggest non-modifiable risk factor for cardiovascular disease. The biological, structural and mechanical changes in senescent cardiovascular system are thought to contribute in increasing incidence of cardiovascular disease in aging. Understanding the mechanisms contributing to such changes is therefore crucial for both prevention and development of treatment for cardiovascular diseases.KEYWORDS: cardiovascular aging, mitochondria, telomeres, sirtuin, stem cells

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Up‐regulation of plasma membrane‐associated redox activities in neuronal cells lacking functional mitochondria

Cited by 61 publications

References 68 publications

Mechanisms Underlying Caloric Restriction and Lifespan Regulation

Mechanisms Underlying Caloric Restriction and Lifespan Regulation

Insulin-like growth factor-1 receptor activation prevents hydrogen peroxide-induced oxidative stress, mitochondrial dysfunction and apoptosis

Molecular Mechanisms of Cardiovascular Aging

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