scholarly journals The Epigenetic Link between Polyphenols, Aging and Age-Related Diseases

Genes ◽  
2020 ◽  
Vol 11 (9) ◽  
pp. 1094
Author(s):  
Itika Arora ◽  
Manvi Sharma ◽  
Liou Y. Sun ◽  
Trygve O. Tollefsbol

Aging is a complex process mainly categorized by a decline in tissue, cells and organ function and an increased risk of mortality. Recent studies have provided evidence that suggests a strong association between epigenetic mechanisms throughout an organism’s lifespan and age-related disease progression. Epigenetics is considered an evolving field and regulates the genetic code at several levels. Among these are DNA changes, which include modifications to DNA methylation state, histone changes, which include modifications of methylation, acetylation, ubiquitination and phosphorylation of histones, and non-coding RNA changes. As a result, these epigenetic modifications are vital targets for potential therapeutic interventions against age-related deterioration and disease progression. Dietary polyphenols play a key role in modulating these modifications thereby delaying aging and extending longevity. In this review, we summarize recent advancements linking epigenetics, polyphenols and aging as well as critical findings related to the various dietary polyphenols in different fruits and vegetables. In addition, we cover studies that relate polyphenols and their epigenetic effects to various aging-related diseases such as cardiovascular diseases, neurodegenerative diseases, autoimmune disorders, diabetes, osteoporosis and cancer.

2017 ◽  
Vol 313 (4) ◽  
pp. F835-F841 ◽  
Author(s):  
Cierra N. Sharp ◽  
Leah J. Siskind

Cisplatin is a potent chemotherapeutic used for the treatment of many types of cancer. However, its dose-limiting side effect is nephrotoxicity leading to acute kidney injury (AKI). Patients who develop AKI have an increased risk of mortality and are more likely to develop chronic kidney disease (CKD). Unfortunately, there are no therapeutic interventions for the treatment of AKI. It has been suggested that the lack of therapies is due in part to the fact that the established mouse model used to study cisplatin-induced AKI does not recapitulate the cisplatin dosing regimen patients receive. In recent years, work has been done to develop more clinically relevant models of cisplatin-induced kidney injury, with much work focusing on incorporation of multiple low doses of cisplatin administered over a period of weeks. These models can be used to recapitulate the development of CKD after AKI and, by doing so, increase the likelihood of identifying novel therapeutic targets for the treatment of cisplatin-induced kidney injury.


Author(s):  
Isabela Monique Fortunato ◽  
Tanila Wood dos Santos ◽  
Lucio Fábio Caldas Ferraz ◽  
Juliana Carvalho Santos ◽  
Marcelo Lima Ribeiro

Obesity is a complex chronic disease characterized by excess of body fat. It represents a significant public health problem due to the health-related risk factors. There are growing evidences showing that maternal obesity can program the offspring, which influence neonatal phenotype and predispose offspring to a higher prevalence of metabolic disorders such as obesity. This increased risk may also be epigenetically transmitted across generations. Thus, there is an urgent need to find effective reprogramming approaches in order to resume normal fetal development. Polyphenols are bioactive compounds found in fruits and vegetables that exert their anti-obesity effect through its powerful anti-oxidant and anti-inflammatory activities. Polyphenols supplementation has been proven to counteract the deleterious effects of maternal obesity programming on offspring. Indeed, some polyphenols can cross the placenta and protect the fetal predisposition against obesity. The present review summarizes the effects of dietary polyphenols on obesity-induced maternal reprogramming as an offspring anti-obesity approach.


2010 ◽  
Vol 2010 ◽  
pp. 1-8 ◽  
Author(s):  
Victoria K. Shanmugam ◽  
Virginia D. Steen

Scleroderma is a disease characterized by immune activation, vasculopathy, fibroblast stimulation, and connective tissue fibrosis. End-organ damage occurs due to progressive tissue fibrosis and vasculopathy. Markers of incipient vasculopathy have not been well studied in scleroderma. However, reduced renal functional reserve and proteinuria are common indicators of progressive vasculopathy in diabetic and hypertensive vasculopathy. Recent studies suggest a strong association between renal involvement and outcomes in scleroderma, with a threefold increased risk of mortality from pulmonary hypertension if renal insufficiency is present. We review the types of renal involvement seen in scleroderma and the data to support the use of renal parameters including proteinuria, glomerular filtration rate, and renal vascular dynamics measured with Doppler ultrasound to identify subclinical renal insufficiency. Further studies are warranted to investigate the use of renal parameters as prognostic indicators in scleroderma.


Thorax ◽  
2019 ◽  
Vol 75 (1) ◽  
pp. 78-80 ◽  
Author(s):  
Ganesh Raghu ◽  
Brett Ley ◽  
Kevin K Brown ◽  
Vincent Cottin ◽  
Kevin F Gibson ◽  
...  

In this retrospective study of a randomised trial of simtuzumab in idiopathic pulmonary fibrosis (IPF), prodromal decline in forced vital capacity (FVC) was significantly associated with increased risk of mortality, respiratory and all-cause hospitalisations, and categorical disease progression. Predictive modelling of progression-free survival event risk was used to assess the effect of population enrichment for patients at risk of rapid progression of IPF; C-index values were 0.64 (death), 0.69 (disease progression), and 0.72 (adjudicated respiratory hospitalisation) and 0.76 (all-cause hospitalisation). Predictive modelling may be a useful tool for improving efficiency of clinical trials with categorical end points.


2018 ◽  
Vol 72 (8) ◽  
pp. 711-714 ◽  
Author(s):  
James White ◽  
Giles Greene ◽  
Mika Kivimaki ◽  
G David Batty

BackgroundTo examine the combined influence of changes in physical activity, diet, smoking and alcohol consumption on all-cause mortality.MethodsHealth behaviours were assessed in 1984/1985 and 1991/1992 in 8123 adults from the UK (4666 women, median age 41.0 years). An unhealthy lifestyle score was calculated, allocating one point for smoking, fruits and vegetables <3 times a day, physical activity <2 hours a week and >14 units (women) or >21 units of alcohol (men) per week.ResultsThere were 2003 deaths over a median follow-up of 6.6 years (IQR 5.9–7.2) following the resurvey. The modal change in the unhealthy lifestyle score was zero, 41.8% had the same score, 35.5% decreased and 22.7% increased score between surveys. A one unit decrease in the unhealthy lifestyle score was not associated with a beneficial effect on mortality (HR 0.93; 95% CI 0.83 to 1.04). A one unit increase in the unhealthy lifestyle score increased the risk of mortality (adjusted HR 1.09; 95% CI 1.01 to 1.18).ConclusionsIn this general population sample, the adoption of an unhealthy lifestyle was associated with an increased risk of mortality.


2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Ching-Yu Cheng ◽  
Kenji Yamashiro ◽  
Li Jia Chen ◽  
Jeeyun Ahn ◽  
Lulin Huang ◽  
...  

Abstract Age-related macular degeneration (AMD) is a major cause of blindness, but presents differently in Europeans and Asians. Here, we perform a genome-wide and exome-wide association study on 2,119 patients with exudative AMD and 5,691 controls, with independent replication in 4,226 patients and 10,289 controls, all of East Asian descent, as part of The Genetics of AMD in Asians (GAMA) Consortium. We find a strong association between CETP Asp442Gly (rs2303790), an East Asian-specific mutation, and increased risk of AMD (odds ratio (OR)=1.70, P=5.60 × 10−22). The AMD risk allele (442Gly), known to protect from coronary heart disease, increases HDL cholesterol levels by 0.17 mmol l−1 (P=5.82 × 10−21) in East Asians (n=7,102). We also identify three novel AMD loci: C6orf223 Ala231Ala (OR=0.78, P=6.19 × 10−18), SLC44A4 Asp47Val (OR=1.27, P=1.08 × 10−11) and FGD6 Gln257Arg (OR=0.87, P=2.85 × 10−8). Our findings suggest that some of the genetic loci conferring AMD susceptibility in East Asians are shared with Europeans, yet AMD in East Asians may also have a distinct genetic signature.


Author(s):  
Mert Esme ◽  
Meltem Koca ◽  
Ayse Dikmeer ◽  
Cafer Balci ◽  
Naim Ata ◽  
...  

Abstract Background A novel coronavirus (severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2]) occurred in China in December 2019 and has spread globally. In this study, we aimed to describe the clinical characteristics and outcomes of hospitalized older adults with coronavirus disease 2019 (COVID-19) in Turkey. Methods We retrospectively analyzed the clinical data of hospitalized patients aged ≥ 60 years with confirmed COVID-19 from March 11, 2020 to May 27, 2020 using nationwide health database. Results In this nationwide cohort, a total of 16,942 hospitalized older adults with COVID-19 were enrolled, of whom 8,635 (51%) were women. Mean age was 71.2 ± 8.5 years, ranging from 60 to 113 years. Mortality rate before and after curfew was statistically different (32.2% vs. 17.9%; p &lt; .001, respectively). Through multivariate analysis of the causes of death in older patients, we found that male gender, diabetes mellitus, heart failure, dementia, were all significantly associated with mortality in entire cohort. In addition to abovementioned risk factors, in patients aged between 60 and 79 years, hypertension, chronic kidney disease and cancer and in patients 80 years of age and older malnutrition were also associated with increased risk of mortality. Conclusions In addition to the results of previous studies with smaller sample size, our results confirmed the age-related relationship between specific comorbidities and COVID-19–related mortality.


2021 ◽  
Author(s):  
Mohsen Moghoofei ◽  
Shayan Mostafaei ◽  
Nasim Kondori ◽  
Michelle E. Armstrong ◽  
Farhad Babaei

Abstract BackgroundIdiopathic pulmonary fibrosis (IPF) is a progressive interstitial pneumonia of unknown etiology with a mean survival rate of less than 3 years. Gap StatementNo previous studies have been performed on the role of co-infection (viral and bacterial infection) in the pathogensis and progression of IPF.AimIn this study, we investigated the role of viral/bacterial infection and coinfection and their possible association with pathogensis and progression of IPF.MethodsWe investigated the prevalence and impact of bacterial and viral coinfection in IPF patients (n = 67) in the context of pulmonary function (FVC, FEV1 and DLCO), disease status and mortality risk. Using principal component analysis (PCA), we also investigated the relationship between and distribution of bacterial and viral co-infection in the IPF cohort.ResultsOf the 67 samples, 17.9% samples were positive for viral infection, 10.4% samples were positive for bacterial infection and 59.7% samples were positive coinfection. We demonstrated that IPF patients who were co-infected had a significantly increased risk of mortality compared (p = 0.031) with IPF patients who were non-infected [Hazard ratio: 8.12; 95% C.I.: 1.3–26.9]. Furthermore, coinfection has also been implicated in disease progression during acute exacerbations in IPF (AE-IPF).ConclusionIn this study, we report for the first time that IPF patients who were coinfected with bacteria and viral infection have significantly decreased FVC and DLCO (% predicted), increased incidence of AE-IPF, increased incidence of death and risk of mortality compared with non-infected IPF patients.


2017 ◽  
Vol 61 (3) ◽  
pp. 317-324 ◽  
Author(s):  
Rebecca Josefson ◽  
Rebecca Andersson ◽  
Thomas Nyström

Ageing can be defined as a gradual decline in cellular and physical functions accompanied by an increased sensitivity to the environment and risk of death. The increased risk of mortality is causally connected to a gradual, intracellular accumulation of so-called ageing factors, of which damaged and aggregated proteins are believed to be one. Such aggregated proteins also contribute to several age-related neurodegenerative disorders e.g. Alzheimer’s, Parkinson’s, and Huntington’s diseases, highlighting the importance of protein quality control (PQC) in ageing and its associated diseases. PQC consists of two interrelated systems: the temporal control system aimed at refolding, repairing, and/or removing aberrant proteins and their aggregates and the spatial control system aimed at harnessing the potential toxicity of aberrant proteins by sequestering them at specific cellular locations. The accumulation of toxic conformers of aberrant proteins during ageing is often declared to be a consequence of an incapacitated temporal PQC system—i.e. a gradual decline in the activity of chaperones and proteases. Here, we review the current knowledge on PQC in relation to ageing and highlight that the breakdown of both temporal and spatial PQC may contribute to ageing and thus comprise potential targets for therapeutic interventions of the ageing process.


2007 ◽  
Vol 177 (4S) ◽  
pp. 497-497
Author(s):  
James Armitage ◽  
Nokuthaba Sibanda ◽  
Paul Cathcart ◽  
Mark Emberton ◽  
Jan Van Der Meulen

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