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DNA damage is one of the research hotspots in the field of aging and related diseases, because it can cause cell cycle arrest and apoptosis, accelerate the body's rate of aging and increase the risk of aging-related diseases.This review will summarize the mechanisms of DNA damage in cells, animal models and individuals and its associations with aging and aging-related diseases, including cancer, cardiovascular disease, Alzheimer's disease and premature aging syndromes.We aim to provide a theoretical framework for anti-aging research and clinical intervention in the treatment of aging-related diseases.
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Aging begins in the early stages of life and is an irreversible process in which wide-ranging and gradual functional declines occur with age in various organs of the body.Vascular aging, as a part of the overall aging process, plays an important role in the occurrence and development of vascular senescence-related diseases.Autophagy maintains homeostasis of the intracellular environment via degradation of damaged, denatured, or senescent proteins and organelles.Studies have found that basal autophagy is critical in regulating normal vascular function.However, abnormal autophagy may contribute to vascular aging and diseases associated with it.The purpose of this paper is to review recent progress on autophagy in vascular aging and its related diseases.
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Aging is the primary risk factor for many of the most common chronic diseases. The association of cellular senescence with aging-associated conditions has gaining increasing attention. There is now considerable evidence that senescent cell accumulation is an underlying mechanism of aging and age-related diseases. Senescent cells have been emerging as a target for new therapeutic strategies against aging-related pathology. Herein, we review the evidence that cellular senescence drives age-related deterioration and senolytics produce beneficial effect by selective elimination of senescent cells.
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Inflammaging is the chronic, systematic, and controllable upregulation of a pro-inflammation state with advancing age. Chronic low-grade inflammation accompanied by sustained stimuli is correlated with various age-related diseases (ARDs). Recent studies on ARDs have prompted further research interest in the inner mechanisms underlying inflammaging to establish prevention and treatment plans for inflammatory diseases. In this article, we discuss inflammaging and its significant role in periodontitis.
Assuntos
Humanos , Envelhecimento , Inflamação , Periodontite , Alergia e ImunologiaRESUMO
TP53, a tumor suppressor gene, has a critical role in cell cycle, apoptosis and cell senescence and participates in many crucial physiological and pathological processes. Identification of TP53 polymorphism in older people and age-related diseases may provide an understanding of its physiology and pathophysiological role as well as risk factors for complex diseases. TP53 codon 72 (TP53:72) polymorphism was investigated in 383 individuals aged 66 to 97 years in a cohort from a Brazilian Elderly Longitudinal Study. We investigated allele frequency, genotype distribution and allele association with morbidities such as cardiovascular disease, type II diabetes, obesity, neoplasia, low cognitive level (dementia), and depression. We also determined the association of this polymorphism with serum lipid fractions and urea, creatinine, albumin, fasting glucose, and glycated hemoglobin levels. DNA was isolated from blood cells, amplified by PCR using sense 5'-TTGCCGTCCCAAGCAATGGATGA-3' and antisense 5'-TCTGGGAAGGGACAGAAGATGAC-3' primers and digested with the BstUI enzyme. This polymorphism is within exon 4 at nucleotide residue 347. Descriptive statistics, logistic regression analysis and Student t-test using the multiple comparison test were used. Allele frequencies, R (Arg) = 0.69 and P (Pro) = 0.31, were similar to other populations. Genotype distributions were within Hardy-Weinberg equilibrium. This polymorphism did not show significant association with any age-related disease or serum variables. However, R allele carriers showed lower HDL levels and a higher frequency of cardiovascular disease than P allele subjects. These findings may help to elucidate the physiopathological role of TP53:72 polymorphism in Brazilian elderly people.