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Biogerontology
Journal Prestige (SJR): 1.428  Citation Impact (citeScore): 3 Number of Followers: 1  Hybrid journal (It can contain Open Access articles)ISSN (Print) 1573-6768 - ISSN (Online) 1389-5729 Published by Springer-Verlag  [2469 journals]
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- The glutamate/GABA system in the retina of male rats: effects of aging,
neurodegeneration, and supplementation with melatonin and antioxidant SkQ1
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Abstract: Abstract Glutamate and -aminobutyric acid (GABA) are the most abundant amino acids in the retina. An imbalance of the glutamate/GABA system is involved in the pathogenesis of various neurodegenerative disorders. Here we for the first time analyzed alterations of expression of glutamate- and GABA-synthesizing enzymes, transporters, and relevant receptors in the retina with age in Wistar rats and in senescence-accelerated OXYS rats who develop AMD-like retinopathy. We noted consistent age-dependent expression changes of GABAergic-system proteins (GAD67, GABA-T, and GAT1) in OXYS and Wistar rats: upregulation by age 3 months and downregulation at age 18 months. At a late stage of AMD-like retinopathy in OXYS rats (18 months), there was significant upregulation of glutaminase and downregulation of glutamine synthetase, possibly indicating an increasing level of glutamate in the retina. AMD-like-retinopathy development in the OXYS strain was accompanied by underexpression of glutamate transporter GLAST. Prolonged supplementation with both melatonin and SkQ1 (separately) suppressed the progression of the AMD-like pathology in OXYS rats without affecting the glutamate/GABA system but worsened the condition of the Wistar rat's retina during normal aging. We observed decreasing protein levels of glutamine synthetase, GLAST, and GABAAR1 and an increasing level of glutaminase in Wistar rats. In summary, both melatonin and mitochondrial antioxidant SkQ1 had different effect on the retinal glutamate / GABA in healthy Wistar and senescence-accelerated OXYS rats.
PubDate: 2022-08-15
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- Long-term sulforaphane-treatment restores redox homeostasis and prevents
cognitive decline in middleaged female and male rats, but cannot revert
previous damage in old animals-
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Abstract: Abstract Aging is a complex and detrimental process, which disrupts most organs and systems within the organisms. The nervous system is morphologically and functionally affected during normal aging, and oxidative stress has been involved in age-related damage, leading to cognitive decline and neurodegenerative processes. Sulforaphane (SFN) is a hormetin that activates the antioxidant and anti-inflammatory responses. So, we aimed to evaluate if SFN long-term treatment was able to prevent age-associated cognitive decline in adult and old female and male rats. Memory was evaluated in adult (15-month-old), and old (21-month-old) female and male Wistar rats after three months of SFN treatment. Young rats (4-month-old) were used as age controls. The antioxidant response induction, the redox state (GSH/GSSG), and oxidative damage were determined in the brain cortex (Cx) and hippocampus (Hc). Our results showed that SFN restored redox homeostasis in the Cx and Hc of adult rats, thus preventing cognitive decline in both sexes; however, the redox responses were not the same in males and females. Old rats were not able to recover their redox state as adults did, but they had a mild improvement. These results suggest that SFN mainly prevents rather than reverts neural damage; though, there might also be a range of opportunities to use hormetins like SFN, to improve redox modulation in old animals.
PubDate: 2022-08-12
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- Hormetic association between perceived stress and human epigenetic aging
based on resilience capacity-
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Abstract: Abstract Chronic stress is associated with deleterious health outcomes and mortality risk. A potential mechanism by which stress affects healthspan and lifespan is acceleration of cellular aging. Biologic age prediction models, termed epigenetic clocks, have been developed to estimate biologic age differences among people with the same chronologic age. This study evaluates the simultaneous impact of perceived chronic stress and resilience on Grim Age acceleration. The perceived stress score (PSS) and Connor-Davidson Resilience Scale (CD-RISC) were used to measure chronic stress and resilience, respectively. DNA was extracted from whole blood and analyzed using the MethylationEPIC BeadChip. GrimAge estimates were calculated using the methylation age calculator. Forty-seven business executives were categorized by levels of high or low stress and resilience scores. Compared to participants with low stress and high resilience, those with low stress and low resilience demonstrated the strongest association with Grim Age acceleration (p = 0.044), after controlling for age and estimated cellular proportions. Interestingly, among participants with low resilience, those with high perceived stress had a weaker association with Grim Age acceleration than participants with low perceived stress. However, among participants with high resilience, low perceived stress had a weaker association with Grim Age acceleration than high perceived stress. Our findings suggest that the impact of perceived stress on epigenetic age acceleration may differ based on resilience capacity, with a potential paradoxical beneficial effect among those with low resilience.
PubDate: 2022-08-12
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- Ginseng volatile oil prolongs the lifespan and healthspan of
Caenorhabditis elegans-
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Abstract: Abstract Ginseng volatile oil (GVO) is one of the main components of ginseng and has antibacterial and anti-inflammatory properties. In this study, gas chromatography–mass spectrometry (GC–MS) was applied to characterize GVO chemical composition, and 73 volatile components were detected from GVO. Caenorhabditis elegans was used as animal model to further elucidate the antioxidant and anti-aging effects of GVO in vivo. The results suggested that GVO significantly prolonged the lifespan of C. elegans and promoted its health without damaging its reproductive capacity. In addition, GVO increased the antioxidant capacity and survival rate of nematodes after heat shock. Transcriptional sequencing showed that autophagy-related genes atg-4.2, atg-7, lgg-2, and cyd-1 were up-regulated, and superoxide dismutase 1 (sod-1) expression was increased after GVO pretreatment. Considering the role of autophagy and antioxidant in aging, the expression of autophagy substrate P62 protein in BC12921 strain was analyzed and found to decrease by more than 50.00% after treatment with GVO. In addition, the lifespan of SOD-1 mutant nematodes was not significantly different from that of the control group. SOD activity and autophagy were activated, which is a clear expression of hormesis. All these results suggest that GVO prolongs the lifespan and healthspan of C. elegans, and its biological functions may be related to hormesis.
PubDate: 2022-08-08
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- High stability of blood parameters during mouse lifespan: sex-specific
effects of every-other-day fasting-
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Abstract: Abstract Every-other-day fasting (EODF) is one type of caloric restriction that is proposed to have significant health benefits, including slowing aging-related processes. The present study evaluated multiple parameters of blood homeostasis comparing mice of different ages and mice on different diet regimes: ad libitum (AL) versus EODF. Hematological and classical biochemical parameters of blood were measured in young (6-month), middle-aged (12-month) and old (18-month) C57BL/6J mice of both sexes subjected either to EODF, or AL feeding. Middle-aged AL males showed a decrease in erythrocyte and total leucocyte counts and an increase in plasma alkaline phosphatase activity, whereas old animals showed a decrease in relative levels of lymphocytes and an increase in relative levels of neutrophils, a decrease in plasma lactate and an increase in total cholesterol levels, compared to young mice. AL-fed females demonstrated higher stability of blood parameters during aging than males did. The EODF regimen did not significantly affect hematological parameters in females but prevented a decline in total leukocyte count with age in males. In both sexes, EODF partially prevented age-associated changes in levels of plasma lactate and cholesterol and activity of alkaline phosphatase. Thus, during normal aging, mice showed a sex-dependent maintenance of blood homeostasis which was not significantly affected by EODF.
PubDate: 2022-08-01
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- Melatonin-related signaling pathways and their regulatory effects in aging
organisms-
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Abstract: Abstract Melatonin is a tryptophan-derived ancestral molecule evolved in bacteria. According to the endosymbiotic theory, eukaryotic cells received mitochondria, plastids, and other organelles from bacteria by internalization. After the endosymbiosis, bacteria evolved into organelles and retained their ability of producing melatonin. Melatonin is a small, evolutionarily conserved indole with multiple receptor-mediated, receptor-dependent, and independent actions. Melatonin’s initial function was likely a radical scavenger in bacteria that’s why there was high intensity of free radicals on primitive atmosphere in the ancient times, and hormetic functions of melatonin, which are effecting through the level of gene expression via prooxidant and antioxidant redox pathways, are developed in throughout the eukaryotic evolution. In the earlier stages of life, endosymbiotic events between mitochondria and other downstream organelles continue with mutual benefits. However, this interaction gradually deteriorates as a result of the imperfection of both mitochondrial and extramitochondrial endosymbiotic crosstalk with the advancing age of eukaryotic organisms. Throughout the aging process melatonin levels tend to reduce and as a manifestation of this, many symptoms in organisms’ homeostasis, such as deterioration in adjustment of cellular clocks, are commonly seen. In addition, due to deterioration in mitochondrial integrity and functions, immunity decreases, and lower levels of melatonin renders older individuals to be more susceptible to impaired redox modulation and age-related diseases. Our aim in this paper is to focus on the several redox modulation mechanisms in which melatonin signaling has a central role, to discuss melatonin’s gerontological aspects and to provide new research ideas with researchers.
PubDate: 2022-07-27
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- Level-dependent effects of predation stress on prey development, lifespan
and reproduction in mites-
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Abstract: Abstract In predator–prey interactions, non-consumptive effects of predators have been less studied than consumptive effects. However, non-consumptive effects may have significant influences on prey and can change different aspects of their life history such as development, reproduction and lifespan. The odour and other cues associated with a predator, without direct contact, could induce stress in prey, leading to phenotypic changes in life history traits. In this study, we investigate how mild and strong predator-induced stress could affect prey life history. The prey (Tyrophagus putrescentiae) was exposed, from hatching to death, to three different levels of predation stress from its predator (Neoseiulus cucumeris) (1, 3 or 5 predator adults in an adjacent cage separated by a mesh screen). Compared with the control, both males and females under predator-induced stress had longer developmental time and shorter lifespan when the level of predation stress increased, showing significant level-dependence. In addition, females had reduced fecundity under predation stress. Sex-specific response to predation stress was observed under a low level of predation stress: females had greater reduction in lifespan than males. Furthermore, the reduction in female lifespan was due more from the decrease in the post-oviposition period than the decrease in the oviposition period. Future studies applying even milder levels of predation press, such as exposure of prey to predator cues only during part of the prey lifespan, may provide additional insights.
PubDate: 2022-07-25
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- Role of H4K16 acetylation in 53BP1 recruitment to double-strand break
sites in in vitro aged cells-
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Abstract: Abstract Increased frequency of DNA double strand breaks (DSBs) with aging suggests an age-associated decline in DSB repair efficiency, which is also influenced by the epigenetic landscape. H4 acetylation at lysine 16 (H4K16Ac) has been related to DSB repair since deacetylation of this mark is required for efficient 53BP1 recruitment to DSBs. Although age-associated changes in H4K16Ac levels have been studied, their contribution to age-related DSB accumulation remains unknown. In vitro aged Human Dermal Fibroblasts (HDFs) display lower levels of H4K16A that correlate with reduced recruitment of 53BP1 to basal DSBs. Following DNA damage induction, early passage (EP) cells suffered from a transient H4K16 deacetylation that allowed proper 53BP1 recruitment to DSBs. In contrast, to reach this specific and optimum level, aged cells responded by increasing their overall lower H4K16Ac levels. Induced hyperacetylation of late passage (LP) cells using trichostatin A increased H4K16Ac levels but did not ameliorate 53BP1 recruitment. Instead, deacetylation induced by MOF silencing reduced H4K16Ac levels and compromised 53BP1 recruitment in both EP and LP cells. Age-associated decrease of H4K16Ac levels contributes to the repair defect displayed by in vitro aged cells. H4K16Ac responds to DNA damage in order to reach a specific, optimum level that allows proper 53BP1 recruitment. This response may be compromised with age, as LP cells depart from lower H4K16Ac levels. Variations in H4K16Ac following the activation of the DNA damage response and aging point at this histone mark as a key mediator between DNA repair and age-associated chromatin alterations.
PubDate: 2022-07-18
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- Mitochondrial function and nutrient sensing pathways in ageing: enhancing
longevity through dietary interventions-
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Abstract: Abstract Ageing is accompanied by alterations in several biochemical processes, highly influenced by its environment. It is controlled by the interactions at various levels of biological hierarchy. To maintain homeostasis, a number of nutrient sensors respond to the nutritional status of the cell and control its energy metabolism. Mitochondrial physiology is influenced by the energy status of the cell. The alterations in mitochondrial physiology and the network of nutrient sensors result in mitochondrial damage leading to age related metabolic degeneration and diseases. Calorie restriction (CR) has proved to be as the most successful intervention to achieve the goal of longevity and healthspan. CR elicits a hormetic response and regulates metabolism by modulating these networks. In this review, the authors summarize the interdependent relationship between mitochondrial physiology and nutrient sensors during the ageing process and their role in regulating metabolism.
PubDate: 2022-07-16
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- Swimming exercise with l-arginine coated nanoparticles supplementation
upregulated HAND2 and TBX5 expression in the cardiomyocytes of aging male
rats-
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Abstract: Abstract We investigated possible cardioprotective mechanisms of l-arginine coated nanoparticles (L-ACN) combined with swimming exercise (SE) in aging male rats considering heart and neural crest derivatives-expressed protein 2 (HAND2) and t-box transcription factor 5 (TBX5). Thirty-five male Wistar rats were randomly assigned into five groups: young, old, old + L-ACN, old + SE, and old + L-ACN + SE (n = 7 in each). l-arginine coated with chitosan nanoparticles was given to L-ACN groups via gavage at 500 mg/kg/day. SE groups performed a swimming exercise program 5 days per week for 6 weeks. The exercise program started with 20 min, gradually increasing to 60 min after four sessions, which was then constant until the completion of the training period. After the protocol completion, the rats were sacrificed, and the heart was fixed and frozen to carry out histological, immunohistochemistry (IHC), and gene expression analyses. The expression of HAND2 protein, HAND2 mRNA, and TBX5 mRNA of the heart tissue was significantly higher in the young group than in all older groups (P < 0.05). The old + L-ACN, old + SE, and old + L-ACN + SE groups showed a significant increase in these factors compared to the old group (P < 0.05). Nano-l-arginine supplement, along with swimming exercises, seems to have cardioprotective potential and improve cardiac function in old age by strengthening cardiomyocyte signaling, especially HAND2 and TBX5. However, more research is required, particularly on human samples.
PubDate: 2022-07-09
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- Exploring the fuzzy border between senolytics and senomorphics with
chemoinformatics and systems pharmacology-
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Abstract: Abstract Senescent cells accumulate within tissues during aging and secrete an array of pro-inflammatory molecules known as senescent-associated secretory phenotype (SASP), which contribute to the appearance and progression of various chronic degenerative diseases. Novel pharmacological approaches aimed at modulating or eliminating senescent cells´ harmful effects have recently emerged: Senolytics are molecules that selectively eliminate senescent cells, while senomorphics modulate or decrease the inflammatory response to specific SASP. So far, the physicochemical, structural, and pharmacological properties that define these two kinds of pharmacological approaches remain unclear. Therefore, the identification and correct choice of molecules, based on their physicochemical, structural, and pharmacological properties, likely to exhibit the desired senotherapeutic activity is crucial for developing effective, selective, and safe senotherapies. Here we compared the physicochemical, structural, and pharmacological properties of 84 senolytics and 79 senomorphics using a chemoinformatic and systems pharmacology approach. We found great physicochemical, structural, and pharmacological similarities between them, also reflected in their cellular responses measured through transcriptome perturbations. The identified similarities between senolytics and senomorphics might explain the dual activity of some of those molecules. These findings will help design and discover new, more effective, and highly selective senotherapeutic agents.
PubDate: 2022-07-04
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- Mitochondria-targeted senotherapeutic interventions
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Abstract: Abstract Healthy aging is the art of balancing a delicate scale. On one side of the scale, there are the factors that make life difficult with aging, and on the other side are the products of human effort against these factors. The most important factors that make the life difficult with aging are age-related disorders. Developing senotherapeutic strategies may bring effective solutions for the sufferers of age-related disorders. Mitochondrial dysfunction comes first in elucidating the pathogenesis of age-related disorders and presenting appropriate treatment options. Although it has been widely accepted that mitochondrial dysfunction is a common characteristic of cellular senescence, it still remains unclear why dysfunctional mitochondria occupy a central position in the development senescence-associated secretory phenotype (SASP) related to age-related disorders. Mitochondrial dysfunction and SASP-related disease progression are closely interlinked to weaken immunity which is a common phenomenon in aging. A group of substances known as senotherapeutics targeted to senescent cells can be classified into two main groups: senolytics (kill senescent cells) and senomorphics/senostatics (suppress their SASP secretions) in order to extend health lifespan and potentially lifespan. As mitochondria are also closely related to the survival of senescent cells, using either mitochondria-targeted senolytic or redox modulator senomorphic strategies may help us to solve the complex problems with the detrimental consequences of cellular senescence. Killing of senescent cells and/or ameliorate their SASP-related negative effects are currently considered to be effective mitochondria-directed gerotherapeutic approaches for fighting against age-related disorders.
PubDate: 2022-07-04
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- Green tea EGCG effectively alleviates experimental colitis in middle-aged
male mice by attenuating multiple aspects of oxi-inflammatory stress and
cell cycle deregulation-
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Abstract: Abstract Age-dependent increased risk of inflammatory bowel diseases such as ulcerative colitis is being increasingly realized, and yet therapies targeting this disorder within the purview of aging are limited. The present study attempted to assess the efficacy of green tea epigallocatechin gallate (EGCG) consumption in preventing the severity and progression of dextran sulphate sodium (DSS)-induced ulcerative colitis in 18 months old middle-aged male mice. Acute colitis was induced in animals using DSS and protective effects of EGCG consumption were examined. Different parameters related to disease progression and molecular markers related to oxi-inflammatory stress, localized and systemic cytokine response, epithelial barrier integrity, and cell cycle progression profile were evaluated. DSS treatment induced rapid and severe symptoms of colitis such as consistently increased DAI score, shortened and inflamed colon accompanied by increased levels of inflammatory proteins (TNFα/IL-6/IL-1β) in both the colon tissue and cultured splenocytes indicating exaggerated Th1 immune response. Markers of oxidative stress increased while antioxidant defences and the expression of tight junction genes in the colonic cells were attenuated. Dysregulation in the expression of cell cycle inhibitory genes (p53/p21WAF1/p16Ink4a) indicated possible induction of colitis-induced dysplasia. On the other hand, EGCG consumption strongly attenuated all the measured ostensible as well as molecular markers of the disease progression as evidenced by improved DAI score, cellular antioxidant capacity, attenuated Th1 cytokine response both in the colon and cultured splenocytes, enhanced expression of tight junction genes, and cell cycle inhibitors thereby suggesting systemic effects of EGCG. Together, these observations suggest that drinking EGCG-rich green tea can be a significant way of managing the severity of colitis during aging.
PubDate: 2022-07-02
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- Dietary intervention with Tinospora cordifolia improved aging-related
decline in locomotor coordination and cerebellar cell survival and
plasticity in female rats-
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Abstract: Reduced bone mineral density, and muscle strength are the hallmark of aging-related motor coordination deficits and related neuropathologies. Since cerebellum regulates motor movements and balance perception of our body, therefore it may be an important target to control the age-related progression of motor dysfunctions. Dry stem powder of Tinospora cordifolia (TCP) was tested as a food supplement to elucidate its activity to attenuate age-associated locomotor dysfunctions. Intact acyclic middle-aged female rats were used in this study as the model system of the transition phase from premenopause to menopause in women along with cycling young adult rats. Normal chow or 30% High Fat Diet (HFD), supplemented with or without TCP was fed to animals for 12 weeks and then tested for locomotor performance on rotarod followed by post-sacrifice protein expression studies. In comparison to young adults, middle-aged animals showed an increase in number of falls and lesser time spent in rotarod performance test, whereas, animals given TCP supplemented feed showed improvement in performance with more pronounced effects observed in normal chow than HFD fed middle-aged rats. Further, due to its multicomponent nature TCP was found to target the expression of various markers of neuroinflammation, apoptosis, cell survival, and synaptic plasticity in the cerebellum region. The current findings suggest that TCP supplementation in the diet may prove to be a potential interventional strategy for the management of frailty and fall-associated morbidities caused by aging-related deterioration of bone mineral density, and muscle strength. Graphical abstract
PubDate: 2022-06-29
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- Identification of healthspan-promoting genes in Caenorhabditis elegans
based on a human GWAS study-
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Abstract: Abstract To find drivers of healthy ageing, a genome-wide association study (GWAS) was performed in healthy and unhealthy older individuals. Healthy individuals were defined as free from cardiovascular disease, stroke, heart failure, major adverse cardiovascular event, diabetes, dementia, cancer, chronic obstructive pulmonary disease (COPD), asthma, rheumatism, Crohn’s disease, malabsorption or kidney disease. Six single nucleotide polymorphisms (SNPs) with unknown function associated with ten human genes were identified as candidate healthspan markers. Thirteen homologous or closely related genes were selected in the model organism C. elegans for evaluating healthspan after targeted RNAi-mediated knockdown using pathogen resistance, muscle integrity, chemotaxis index and the activity of known longevity and stress response pathways as healthspan reporters. In addition, lifespan was monitored in the RNAi-treated nematodes. RNAi knockdown of yap-1, wwp-1, paxt-1 and several acdh genes resulted in heterogeneous phenotypes regarding muscle integrity, pathogen resistance, chemotactic behaviour, and lifespan. Based on these observations, we hypothesize that their human homologues WWC2, CDKN2AIP and ACADS may play a role in health maintenance in the elderly.
PubDate: 2022-06-24
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- Tackling cellular senescence by targeting miRNAs
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Abstract: Abstract Cellular senescence, which is characterized by permanent proliferation arrest, has become an important target for the amelioration of various human diseases. The activity of senescent cells is mainly related to the senescence-associated secretory phenotype (SASP). The SASP can cause chronic inflammation in local tissues and organs through autocrine and paracrine mechanisms, and a series of factors secreted by senescent cells can deteriorate the cellular microenvironment, promoting tumor formation and exacerbating aging-related diseases. Therefore, avoiding the promotion of cancer is an urgent problem. In recent years, increased attention has been given to the mechanistic study of microRNAs in senescence. As important posttranscriptional regulators, microRNAs possess unique tissue-specific expression in senescence. MicroRNAs can regulate the SASP by regulating proteins in the senescence signaling pathway, the reverse transcriptase activity of telomerase, the generation of reactive oxygen species and oxidative damage to mitochondria. Numerous studies have confirmed that removing senescent cells does not cause significant side effects, which also opens the door to the development of treatment modalities against senescent cells. Herein, this review discusses the double-edged sword of cellular senescence in tumors and aging-related diseases and emphasizes the roles of microRNAs in regulating the SASP, especially the potential of microRNAs to be used as therapeutic targets to inhibit senescence, giving rise to novel therapeutic approaches for the treatment of aging-associated diseases.
PubDate: 2022-06-21
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- Dietary interventions and molecular mechanisms for healthy musculoskeletal
aging-
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Abstract: Abstract Over the past decade, extensive efforts have focused on understanding age-associated diseases and how to prolong a healthy lifespan. The induction of dietary protocols such as caloric restriction (CR) and protein restriction (PR) has positively affected a healthy lifespan. These intervention ideas (nutritional protocols) have been the subject of human cohort studies and clinical trials to evaluate their effectiveness in alleviating age-related diseases (such as type II diabetes, cardiovascular disease, obesity, and musculoskeletal fragility) and promoting human longevity. This study summarizes the literature on the nutritional protocols, emphasizing their impacts on bone and muscle biology. In addition, we analyzed several CR studies using Gene Expression Omnibus (GEO) database and identified common transcriptome changes to understand the signaling pathway involved in musculoskeletal tissue. We identified nine novel common genes, out of which five were upregulated (Emc3, Fam134b, Fbxo30, Pip5k1a, and Retsat), and four were downregulated (Gstm2, Per2, Fam78a, and Sel1l3) with CR in muscles. Gene Ontology enrichment analysis revealed that CR regulates several signaling pathways (e.g., circadian gene regulation and rhythm, energy reserve metabolic process, thermogenesis) involved in energy metabolism. In conclusion, this study summarizes the beneficiary role of CR and identifies novel genes and signaling pathways involved in musculoskeletal biology.
PubDate: 2022-06-21
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- Correlative links between natural radiation and life expectancy in the US
population-
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Abstract: Abstract The linear no-threshold (LNT) hypothesis is still the ruling concept which dictates the radiation protection health policy and regulations. However, more and more studies show that not only that low dose radiation pose no danger to our health, but also exhibits clear beneficial health effects. Here, we evaluated the correlative links of the natural sources of radiation—terrestrial radiation (TR), cosmic radiation (CR), and Radon-222, with life expectancy, the most integrative index of population health. The results of this study show that the different sources of natural radiation display positive correlative links to life expectancy, which is in line with the hypothesis of radiation hormesis.
PubDate: 2022-06-21
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- Hormesis is an evolutionary expectation: implications for aging
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Abstract: Abstract This article argues that evolution and the concept of hormesis are biologically inseparable. It proposes that evolutionary processes led to the selection of inducible adaptive hormetic strategies that are necessary for wellbeing and survival. Hormesis has been demonstrated in essentially all organisms in which it has been studied from bacteria to humans, showing its highly conserved features. This evolution-hormesis integration should be a central feature in both understanding the biology of aging but also in ways to enhance improved health-based aging strategies.
PubDate: 2022-05-07
DOI: 10.1007/s10522-022-09964-z
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- Retraction Note to: Carbohydrate-restricted diet promotes skin senescence
in senescence-accelerated prone mice-
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PubDate: 2022-04-25
DOI: 10.1007/s10522-022-09963-0
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