Immune System, Cell Senescence, Aging and Longevity - Inflamm-Aging Reappraised

Salvioli, Stefano; Monti, Daniela; Lanzarini, Catia; Conte, Maria; Pirazzini, Chiara; Bacalini, Maria Giulia; Garagnani, Paolo; Giuliani, Cristina; Fontanesi, E.; Ostan, Rita; Bucci, Laura; Sevini, Federica; Yani, Stella Lukas; Barbieri, Anna; Lomartire, Laura; Borelli, Vincenzo; Vianello, Dario; Bellavista, Elena; Martucci, Morena; Cevenini, Elisa; Pini, Elisa; Scurti, Maria; Biondi, Fiammetta; Santoro, Aurelia; Capri, Miriam; Franceschi, Claudio

doi:10.2174/138161213805219531

Cited by 113 publications

(129 citation statements)

References 63 publications

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“…Given that morbid burden increases with age, and that aging itself is associated with increased levels of proinflammatory markers due to immunosenescence [28], one may ask whether an increase in inflammation is a primary contributor to the development of multi-morbidity. To address this possibility, we performed an adjustment of prevalence data for both age and BMI, factors known to both increase with age and contribute to systemic inflammation.…”

Section: Discussionmentioning

confidence: 99%

Age-independent rise of inflammatory scores may contribute to accelerated aging in multi-morbidity

et al. 2015

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Aging is associated with an increase in a chronic, low-grade inflammation. This phenomenon, termed “inflammaging” is also a risk factor for both morbidity and mortality in the elderly. Frequent co-occurrence of chronic diseases, known as multi-morbidity, may be explained by interconnected pathophysiology of these conditions, most of which depend on its inflammatory component. Here we present an analysis of the U.S. National Health and Nutrition Examination Survey data collected between 1999 and 2008, for the presence, and the number, of chronic diseases along with HDL-cholesterol, C-reactive protein, white blood cell count, lymphocyte percent, monocyte percent, segmented neutrophils percent, eosinophils percent, basophils percent, and glycohemoglobin levels. Importantly, even after adjustment for age and BMI, many inflammatory markers continued to be associated to multi-morbidity. C-reactive protein (CRP) levels and Glasgow Prognostic Score (GPS) were most dramatically increased in parallel with an accumulation of chronic diseases, and may be utilized as multi-morbidity predictors. These observations point at background inflammation as direct, age-independent contributor to an accumulation of the disease burden. Our findings also suggest a possibility that systemic inflammation associated with chronic diseases may explain accelerated aging phenomenon previously observed among the patients with heavy disease burden.

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Section: Discussionmentioning

confidence: 99%

Age-independent rise of inflammatory scores may contribute to accelerated aging in multi-morbidity

et al. 2015

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“…CHD is a complex, multifactorial disorder involving multiple environmental risks and genetic factors, and LTL was found to be related to many of these factors 1. CHD is a chronic inflammatory process and the shorter telomere length in individuals prone to CHD could simply indicate a greater white blood cell turnover 16–18. Increased oxidative stress was another factor contributing to atherosclerosis, and increased oxidant stress has been shown to increase rates of telomere attrition in vitro 19–21.…”

Section: Discussionmentioning

confidence: 99%

Association between previously identified loci affecting telomere length and coronary heart disease (CHD) in Han Chinese population

Ding

Zhou

et al. 2014

CIA

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PurposeTo replicate previously confirmed telomere-length loci in a Chinese Han population with coronary heart disease (CHD), and investigate these loci and the possibility of and age at onset of CHD.Patients and methods1514 CHD patients and 2470 normal controls were recruited. Medical data including age, sex, body mass index, lipid profiles, history of hypertension, type 2 diabetes mellitus, and dyslipidemia were collected from all the participants. Seven previously identified single-nucleotide polymorphisms (SNPs) related to leucocyte telomere length were genotyped, including rs10936599 in TERC, rs2736100 in TERT, rs7675998 in NAF1, rs9420907 in OBFC1, rs8105767 in ZNF208, rs755017 in RTEL1, and rs11125529 in ACYP2.ResultsNo significant difference in genotype frequencies from the Hardy–Weinberg equilibrium test was noted for all tested SNPs both in the CHD patients and the normal controls. No polymorphism was observed for rs9420907, and AA genotype was noted in both the CHD patients and the controls. Neither the genotype nor the allele frequencies of rs2736100, rs8105767, rs11125529, and rs2967374 were significantly different between the CHD patients and the normal controls. For rs10936599 and rs755017, statistical difference was found for the allele frequency but not genotype. Distributions of genotype and allele were significantly different between the two groups for rs7675998. The odds ratio for carriers of CHD was 2.127 (95% confidence interval: 1.909–2.370) for the A allele of rs7675998. By one-way analysis of variance test, rs7675998 was associated with the onset age of CHD. CHD patients with the AA genotype of rs7675998 had significantly lower onset age (P<0.05).ConclusionIn a Chinese Han population, NAF1 gene encoding proteins with known function in telomere biology may influence both the possibility of and the age at onset of CHD, as previously reported in European studies.

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“…Aging-associated disruptions of PCD regulation and phagocytosis may contribute to aging-associated inflammation, including activation of the NFκB signaling pathway (Gupta et al, 2006; Salvioli et al, 2013), (Shaw et al, 2010). Because NFκB signaling can be either pro-apoptotic or anti-apoptotic depending on the cellular context, this could couple inflammation to further alterations in PCD in certain tissues.…”

Section: Pcd In Normal Tissue Development Adult Homeostasisand Agingmentioning

confidence: 99%

Programmed cell death in aging

Tower

2015

Ageing Research Reviews

331

208

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Programmed cell death (PCD) pathways, including apoptosis and regulated necrosis, are required for normal cell turnover and tissue homeostasis. Mis-regulation of PCD is increasingly implicated in aging and aging-related disease. During aging the cell turnover rate declines for several highly-mitotic tissues. Aging-associated disruptions in systemic and inter-cell signaling combined with cell-autonomous damage and mitochondrial malfunction result in increased PCD in some cell types, and decreased PCD in other cell types. Increased PCD during aging is implicated in immune system decline, skeletal muscle wasting (sarcopenia), loss of cells in the heart, and neurodegenerative disease. In contrast, cancer cells and senescent cells are resistant to PCD, enabling them to increase in abundance during aging. PCD pathways limit life span in fungi, but whether PCD pathways normally limit adult metazoan life span is not yet clear. PCD is regulated by a balance of negative and positive factors, including the mitochondria, which are particularly subject to aging-associated malfunction.

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Immune System, Cell Senescence, Aging and Longevity - Inflamm-Aging Reappraised

Cited by 113 publications

References 63 publications

Age-independent rise of inflammatory scores may contribute to accelerated aging in multi-morbidity

Age-independent rise of inflammatory scores may contribute to accelerated aging in multi-morbidity

Association between previously identified loci affecting telomere length and coronary heart disease (CHD) in Han Chinese population

Programmed cell death in aging

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