Aging is not a disease: implications for intervention

Rattan, Suresh

doi:10.14336/ad.2014.0500196

Cited by 111 publications

(86 citation statements)

References 89 publications

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“…For example, according to the Encyclopaedia Britannica, ageing is defined as a number of progressive physiological changes in an organism that lead to senescence, or a decline of biological functions and of the organism's ability to adapt to metabolic stress (http://www.britannica.com/ science/aging-life-process). Ageing itself is not a disease (10). It is the normal development of an individual (11).…”

Section: Biological Background Of Ageing and Impact On Cancer Formationmentioning

confidence: 99%

Ageing as an Important Risk Factor for Cancer

et al. 2016

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Section: Biological Background Of Ageing and Impact On Cancer Formationmentioning

confidence: 99%

Ageing as an Important Risk Factor for Cancer

et al. 2016

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“…Although aging is not a disease (330,401), it is recognized as a process that augments the likelihood of disease emergence, particularly of those referred to as age-associated diseases such as hypertension, atherosclerosis and cardiovascular disease, type 2 diabetes, cancer, Alzheimer's disease, osteoporosis, arthritis, cataracts, and neurodegenerative diseases, among others, whose incidences increase progressively with aging (43). Although both age-associated disease and the aging process are linked to derangements of the mTOR, sirtuin, KLOTHO, growth hormone (GH) releasing hormone-GH-IGF-I/insulin, p53, and apolipoprotein E pathways (15) they need to be distinguished as separate entities; however, interventions aimed at targeting the underlying aging process can potentially defer or interrupt the appearance of age-related disease.…”

Section: Updating the Role Of Ros And Mitochondria In Agingmentioning

confidence: 99%

Angiotensin II blockade: how its molecular targets may signal to mitochondria and slow aging. Coincidences with calorie restriction and mTOR inhibition

Cavanagh

Inserra

Ferder

2015

American Journal of Physiology-Heart and Circulatory Physiology

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de Cavanagh EM, Inserra F, Ferder L. Angiotensin II blockade: how its molecular targets may signal to mitochondria and slow aging. Coincidences with calorie restriction and mTOR inhibition. Am J Physiol Heart Circ Physiol 309: H15-H44, 2015. First published May 1, 2015; doi:10.1152/ajpheart.00459.2014, renin angiotensin system blockade (RAS-bl), and rapamycin-mediated mechanistic target of rapamycin (mTOR) inhibition increase survival and retard aging across species. Previously, we have summarized CR and RAS-bl's converging effects, and the mitochondrial function changes associated with their physiological benefits. mTOR inhibition and enhanced sirtuin and KLOTHO signaling contribute to the benefits of CR in aging. mTORC1/mTORC2 complexes contribute to cell growth and metabolic regulation. Prolonged mTORC1 activation may lead to age-related disease progression; thus, rapamycin-mediated mTOR inhibition and CR may extend lifespan and retard aging through mTORC1 interference. Sirtuins by deacetylating histone and transcription-related proteins modulate signaling and survival pathways and mitochondrial functioning. CR regulates several mammalian sirtuins favoring their role in aging regulation. KLOTHO/fibroblast growth factor 23 (FGF23) contribute to control Ca 2ϩ , phosphate, and vitamin D metabolism, and their dysregulation may participate in age-related disease. Here we review how mTOR inhibition extends lifespan, how KLOTHO functions as an aging suppressor, how sirtuins mediate longevity, how vitamin D loss may contribute to age-related disease, and how they relate to mitochondrial function. Also, we discuss how RAS-bl downregulates mTOR and upregulates KLOTHO, sirtuin, and vitamin D receptor expression, suggesting that at least some of RAS-bl benefits in aging are mediated through the modulation of mTOR, KLOTHO, and sirtuin expression and vitamin D signaling, paralleling CR actions in age retardation. Concluding, the available evidence endorses the idea that RAS-bl is among the interventions that may turn out to provide relief to the spreading issue of age-associated chronic disease. mechanistic target of rapamycin; vitamin D; caloric restriction; renin-angiotensin system EFFORTS AIMED AT DECIPHERING the mechanisms that underlie the aging process have unveiled three interventions that can increase survival and retard age-related diseases from lower organisms to mammals, i.e., caloric restriction (CR) (84,85,140,160,334), mechanistic target of rapamycin (mTOR; originally mammalian TOR) inhibition by rapamycin (173,196,281), and renin-angiotensin system blockade (RAS-bl) (20, 21, 26,63,253,284,354), although the latter has been less studied. In light of these findings, some intriguing questions come to mind: Do these interventions attenuate aging by interfering with common mechanisms? Do the mechanisms that are interfered with by CR, rapamycin, and RAS-bl mutually affect each other? Are there any pathways involved exclusively with a certain intervention?Previously (101), we have discussed the converging effects d...

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“…With the increasing elderly population in the world, aging has already become an important public issue (3). Oxidative stress is considered to be significant in the pathophysiology of various diseases, including the aging process.…”

Section: Introductionmentioning

confidence: 99%

Effects of rhein lysinate on D-galactose-induced aging mice

Zhen

Lin

et al. 2015

Experimental and Therapeutic Medicine

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Abstract. The aim of the present study was to investigate the anti-aging effects of rhein lysinate (RHL), and to explore its mechanism of action in a D-galactose-induced aging mouse model. Aging was induced by D-galactose (100 mg/kg/day) that was subcutaneously injected to animals for 8 weeks. RHL was simultaneously administered once a day by intragastric gavage. The appetite, mental condition, body weight and organ index of the mice were monitored. Superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities were determined, and the levels of malondialdehyde (MDA) in the liver, kidney and serum were measured by appropriate assay kits. Western blot analysis was used to detect proteins associated with age. The results indicated that RHL may improve the appetite, mental state and organ conditions of the model mice, improve the activities of SOD and GSH-Px, reduce MDA levels and modulate the expression of age-associated proteins (Sirtuin 1, p21 and p16) in D-galactose-induced mice. Therefore, RHL may be effective at suppressing the aging process through a combination of enhancing antioxidant activity, scavenging free radicals and modulating aging-associated gene expression.

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Aging is not a disease: implications for intervention

Cited by 111 publications

References 89 publications

Ageing as an Important Risk Factor for Cancer

Ageing as an Important Risk Factor for Cancer

Angiotensin II blockade: how its molecular targets may signal to mitochondria and slow aging. Coincidences with calorie restriction and mTOR inhibition

Effects of rhein lysinate on D-galactose-induced aging mice

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