Mechanisms Underlying Caloric Restriction and Lifespan Regulation

Ungvári, Zoltán; Parrado-Fernández, Cristina; Csiszár, Anna; Cabo, Rafael de

doi:10.1161/circresaha.107.168369

Cited by 216 publications

(201 citation statements)

References 165 publications

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“…6 Obese individuals require more calories to maintain their weight and the burning of that extra fuel generates more reactive oxygen species. 8 Men with ED with and without obesity have higher levels of C-reactive protein compared to men with normal erectile function. 6,7,9 Tumor necrosis factor-a, interleukin-6, C-reactive protein and reactive oxygen species all cause insulin resistance.…”

Section: Weight Lossmentioning

confidence: 99%

“…16 Lifestyle, metabolism and erectile function DR Meldrum et al each advancing decade is much lower in the absence of coronary artery disease. 61 Age-related increases of weight, insulin resistance, and oxidative stress and inflammation, 8 and decreases of GSH synthesis, 62 and coital frequency 18 may be some of the mechanisms underlying the association of ED with age in men without coronary artery disease.…”

Section: Agingmentioning

confidence: 99%

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Lifestyle and metabolic approaches to maximizing erectile and vascular health

et al. 2011

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Oxidative stress and inflammation, which disrupt nitric oxide (NO) production directly or by causing resistance to insulin, are central determinants of vascular diseases including ED. Decreased vascular NO has been linked to abdominal obesity, smoking and high intakes of fat and sugar, which all cause oxidative stress. Men with ED have decreased vascular NO and circulating and cellular antioxidants. Oxidative stress and inflammatory markers are increased in men with ED, and all increase with age. Exercise increases vascular NO, and more frequent erections are correlated with decreased ED, both in part due to stimulation of endothelial NO production by shear stress. Exercise and weight loss increase insulin sensitivity and endothelial NO production. Potent antioxidants or high doses of weaker antioxidants increase vascular NO and improve vascular and erectile function. Antioxidants may be particularly important in men with ED who smoke, are obese or have diabetes. Omega-3 fatty acids reduce inflammatory markers, decrease cardiac death and increase endothelial NO production, and are therefore critical for men with ED who are under age 60 years, and/or have diabetes, hypertension or coronary artery disease, who are at increased risk of serious or even fatal cardiac events. Phosphodiesterase inhibitors have recently been shown to improve antioxidant status and NO production and allow more frequent and sustained penile exercise. Some angiotensin II receptor blockers decrease oxidative stress and improve vascular and erectile function and are therefore preferred choices for lowering blood pressure in men with ED. Lifestyle modifications, including physical and penile-specific exercise, weight loss, omega-3 and folic acid supplements, reduced intakes of fat and sugar, and improved antioxidant status through diet and/or supplements should be integrated into any comprehensive approach to maximizing erectile function, resulting in greater overall success and patient satisfaction, as well as improved vascular health and longevity.

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Section: Weight Lossmentioning

confidence: 99%

Section: Agingmentioning

confidence: 99%

Lifestyle and metabolic approaches to maximizing erectile and vascular health

et al. 2011

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“…R edox imbalance between reactive species and endogenous antioxidants, which results in oxidative damage to biologic molecules and impairment in signaling pathways [(i.e., in oxidative stress (145)], has been widely implicated in many ailments, including central nervous system pathologies (46,51,61,122,219,330) [e.g., amyotrophic lateral sclerosis, (46), Parkinson's disease (219), bipolar disorder (330), Alzheimer's disease (61)], cardiovascular conditions (61,112), pulmonary conditions (65,153), diabetes (111,154), eye diseases (19,235), aging (290,323,236), cancer (52,70,317), radiation injury (220), pain=chronic morphine tolerance (89), Fanconi anemia (229). Reactive species, such as nitric oxide ( · NO), superoxide (O 2 ·À ), hydrogen peroxide (H 2 O 2 ), peroxynitrite (ONOO -), and others have been widely recognized as signaling species that, by affecting redox-based cellular transcriptional activity, control inflammatory and immune responses and enhance secondary oxidative stress (27,47,96,151,188,273,276,298,335,336).…”

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confidence: 99%

Superoxide Dismutase Mimics: Chemistry, Pharmacology, and Therapeutic Potential

Batinić‐Haberle

Rebouças

Spasojević

2010

Antioxidants & Redox Signaling

467

689

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Oxidative stress has become widely viewed as an underlying condition in a number of diseases, such as ischemia-reperfusion disorders, central nervous system disorders, cardiovascular conditions, cancer, and diabetes. Thus, natural and synthetic antioxidants have been actively sought. Superoxide dismutase is a first line of defense against oxidative stress under physiological and pathological conditions. Therefore, the development of therapeutics aimed at mimicking superoxide dismutase was a natural maneuver. Metalloporphyrins, as well as Mn cyclic polyamines, Mn salen derivatives and nitroxides were all originally developed as SOD mimics. The same thermodynamic and electrostatic properties that make them potent SOD mimics may allow them to reduce other reactive species such as peroxynitrite, peroxynitrite-derived CO 3 _ À , peroxyl radical, and less efficiently H 2 O 2 . By doing so SOD mimics can decrease both primary and secondary oxidative events, the latter arising from the inhibition of cellular transcriptional activity. To better judge the therapeutic potential and the advantage of one over the other type of compound, comparative studies of different classes of drugs in the same cellular and=or animal models are needed. We here provide a comprehensive overview of the chemical properties and some in vivo effects observed with various classes of compounds with a special emphasis on porphyrin-based compounds. Antioxid. Redox Signal. 13, 877-918.

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“…Therefore, it is conceivable that CR decreased the expression levels of α-tubulin, β-tubulin, and cleaved desmin and restored intact desmin in aged mice, which could be one potential mechanism that prevents the development of aging cardiomyopathy. We also examined oxidative stress, one of the most studied mechanisms mediating the adverse effects of aging (Droge 2002;Harman 1956;Ungvari et al 2008). We examined the antioxidants, MnSOD, and catalase, in long-term CR mice.…”

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confidence: 99%

Calorie restriction can reverse, as well as prevent, aging cardiomyopathy

Yan

Gao

et al. 2013

AGE

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Calorie restriction (CR) is the most widely studied intervention protecting from the adverse effects of aging. Almost all prior studies have examined the effects of CR initiated in young animals. Studies examining the effects of CR on development of aging cardiomyopathy found only partial prevention. The major goal of this study was to determine whether CR initiated after aging cardiomyopathy developed could reverse the cardiomyopathy. Aging cardiomyopathy in 2-year-old mice was characterized by reduced left ventricular (LV) function, cardiac hypertrophy, and increased cardiac apoptosis and fibrosis. When short-term (2 months) CR was initiated after aging cardiomyopathy developed in 20-month-old mice, the decrease in cardiac function, and increases in LV weight, myocardial fibrosis and apoptosis were reversed, such that the aging hearts in these mice were indistinguishable from those of young mice or mice where CR was initiated in young mice. If apoptosis was the mechanism for protecting against aging cardiomyopathy, then total myocyte numbers should have reverted to normal with CR, but did not. However, the alterations in cytoskeletal proteins, which contribute to aging cardiomyopathy, were no longer observed with CR. This is the first study to demonstrate complete prevention of aging cardiomyopathy by CR and, more importantly, that instituting this intervention even later in life can rapidly correct aging cardiomyopathy, which could have important therapeutic implications.

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Mechanisms Underlying Caloric Restriction and Lifespan Regulation

Cited by 216 publications

References 165 publications

Lifestyle and metabolic approaches to maximizing erectile and vascular health

Lifestyle and metabolic approaches to maximizing erectile and vascular health

Superoxide Dismutase Mimics: Chemistry, Pharmacology, and Therapeutic Potential

Calorie restriction can reverse, as well as prevent, aging cardiomyopathy

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