• Journal of Food Hygiene and Safety
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• v.32 no.3
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• pp.243-248
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• 2017

Intracellular and extracellular oxidative stress initiated by reactive oxygen species (ROS) causes skin aging, which is characterized by wrinkles and atypical pigmentation. Use of antioxidant is an effective approach to prevent symptoms related to ROS-induced aging of the skin. Therefore, the antioxidant and anti-aging effect of Castanea crenata Siebold & Zucc. extracts (LCE) was investigated in this study. The LCE markedly reduced the hydrogen peroxide-induced cell damage, intracellular ROS, and oxidative stress-induced senescence in human dermal fibroblasts (HDFs). These results indicate that LCE might have beneficial effects on oxidative stress-induced damage and thus reduce skin aging.

• BMB Reports
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• v.44 no.5
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• pp.291-297
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• 2011

Aging is one of the most complicated biological processes in all species. A number of different model organisms from yeast to monkeys have been studied to understand the aging process. Until recently, many different age-related genes and age-regulating cellular pathways, such as insulin/IGF-1-like signal, mitochondrial dysfunction, Sir2 pathway, have been identified through classical genetic studies. Parallel to genetic approaches, genome-wide approaches have provided valuable insights for the understanding of molecular mechanisms occurring during aging. Gene expression profiling analysis can measure the transcriptional alteration of multiple genes in a genome simultaneously and is widely used to elucidate the mechanisms of complex biological pathways. Here, current global gene expression profiling studies on normal aging and age-related genetic/environmental interventions in widely-used model organisms are briefly reviewed.

• Korean Journal of Biological Psychiatry
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• v.21 no.1
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• pp.1-13
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• 2014

Normal aging causes changes in the brain volume, connection, function and cognition. The brain changes with increases in age and difference of gender varies at all levels. Studies about normal brain aging using various brain magnetic resonance imaging (MRI) variables such as gray and white matter structural imaging, proton spectroscopy, apparent diffusion coefficient, diffusion tensor imaging and functional MRI are reviewed. Total volume of brain increases after birth but decreases after 9 years old. During adulthood, total volume of brain is relatively stable. After 35 years old, brain shrinks gradually. The changes of gray and white matters by aging show different features. N-acetylaspartate decreases or remains unchanged but choline, creatine and myo-inositol increase with aging. Apparent diffusion coefficient decreases till 20 years old and then becomes stable during adulthood and increase after 60 years old. Diffusion tensor properties in white matter tissue are variable during aging. Resting-state functional connectivity decreases after middle age. Structural and functional brain changes with normal aging are important for studying various psychiatric diseases such as dementia, schizophrenia and bipolar disorder. Our review may be helpful for studying longitudinal changes of these diseases and successful aging.

• BMB Reports
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• v.52 no.1
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• pp.13-23
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• 2019

Aging is accompanied by a time-dependent progressive deterioration of multiple factors of the cellular system. The past several decades have witnessed major leaps in our understanding of the biological mechanisms of aging using dietary, genetic, pharmacological, and physical interventions. Metabolic processes, including nutrient sensing pathways and mitochondrial function, have emerged as prominent regulators of aging. Mitochondria have been considered to play a key role largely due to their production of reactive oxygen species (ROS), resulting in DNA damage that accumulates over time and ultimately causes cellular failure. This theory, known as the mitochondrial free radical theory of aging (MFRTA), was favored by the aging field, but increasing inconsistent evidence has led to criticism and rejection of this idea. However, MFRTA should not be hastily rejected in its entirety because we now understand that ROS is not simply an undesired toxic metabolic byproduct, but also an important signaling molecule that is vital to cellular fitness. Notably, mitochondrial function, a term traditionally referred to bioenergetics and apoptosis, has since expanded considerably. It encompasses numerous other key biological processes, including the following: (i) complex metabolic processes, (ii) intracellular and endocrine signaling/communication, and (iii) immunity/inflammation. Here, we will discuss shortcomings of previous concepts regarding mitochondria in aging and their emerging roles based on recent advances. We will also discuss how the mitochondrial genome integrates with major theories on the evolution of aging.

• 보존과학연구
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• s.32
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• pp.137-153
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• 2011

Paper cultural heritages in museums and libraries are deteriorated by many biological factors like as fungi, insects, bacteria and rodents and get irreversibly damaged. Especially, paper components like as cellulose, hemicellulose, lignin, pectins, tannins, proteins and mineral additives are good nourishment for microorganism. Through some studies on fungi causing the aging of paper materials, Aspergilli (about 30%) and Penicilli (more than 30%) are the most common among 300 different kinds of microorganism that caused the biological aging of paper cultural heritages in museums and libraries. At present, various treatments are attempted to control the biodeterioration by these fungi. Especially, it is focused on the control of environmental factors such as humidity, temperature and oxygen. In this study, the oxygen absorbent was used to control oxygen, one of the these favorable conditions during the biological aging of Hanji by Aspergillus versicolor and Penicillium polonicum and then the effect on prevention in aging by this treatment was investigated. In result, the oxygen absorbent treatment had the good effect on prevention in aging during the biological aging by two species of fungi.

• Molecules and Cells
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• v.42 no.12
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• pp.821-827
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• 2019

Aging is the most important single risk factor for many chronic diseases such as cancer, metabolic syndrome, and neurodegenerative disorders. Targeting aging itself might, therefore, be a better strategy than targeting each chronic disease individually for enhancing human health. Although much should be achieved for completely understanding the biological basis of aging, cellular senescence is now believed to mainly contribute to organismal aging via two independent, yet not mutually exclusive mechanisms: on the one hand, senescence of stem cells leads to exhaustion of stem cells and thus decreases tissue regeneration. On the other hand, senescent cells secrete many proinflammatory cytokines, chemokines, growth factors, and proteases, collectively termed as the senescence-associated secretory phenotype (SASP), which causes chronic inflammation and tissue dysfunction. Much effort has been recently made to therapeutically target detrimental effects of cellular senescence including selectively eliminating senescent cells (senolytics) and modulating a proinflammatory senescent secretome (senostatics). Here, we discuss current progress and limitations in understanding molecular mechanisms of senolytics and senostatics and therapeutic strategies for applying them. Furthermore, we propose how these novel interventions for aging treatment could be improved, based on lessons learned from cancer treatment.

• Molecules and Cells
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• v.46 no.7
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• pp.417-419
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• 2023

• Tuberculosis and Respiratory Diseases
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• v.83 no.2
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• pp.107-115
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• 2020

Aging is often viewed as a progressive decline in fitness due to cumulative deleterious alterations of biological functions in the living system. Recently, our understanding of the molecular mechanisms underlying aging biology has significantly advanced. Interestingly, many of the pivotal molecular features of aging biology are also found to contribute to the pathogenesis of chronic lung disorders such as chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis, for which advanced age is the most crucial risk factor. Thus, an enhanced understanding of how molecular features of aging biology are intertwined with the pathobiology of these aging-related lung disorders has paramount significance and may provide an opportunity for the development of novel therapeutics for these major unmet medical needs. To serve the purpose of integrating molecular understanding of aging biology with pulmonary medicine, in this review, recent findings obtained from the studies of aging-associated lung disorders are summarized and interpreted through the perspective of molecular biology of aging.

• Molecules and Cells
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• v.42 no.5
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• pp.379-385
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• 2019

Non-coding RNAs (ncRNAs) comprise various RNA species, including small ncRNAs and long ncRNAs (lncRNAs). ncRNAs regulate various cellular processes, including transcription and translation of target messenger RNAs. Recent studies also indicate that ncRNAs affect organismal aging and conversely aging influences ncRNA levels. In this review, we discuss our current understanding of the roles of ncRNAs in aging and longevity, focusing on recent advances using the roundworm Caenorhabditis elegans. Expression of various ncRNAs, including microRNA (miRNA), tRNA-derived small RNA (tsRNA), ribosomal RNA (rRNA), PIWI-interacting RNA (piRNA), circular RNA (circRNA), and lncRNA, is altered during aging in C. elegans. Genetic modulation of specific ncRNAs affects longevity and aging rates by modulating established aging-regulating protein factors. Because many aging-regulating mechanisms in C. elegans are evolutionarily conserved, these studies will provide key information regarding how ncRNAs modulate aging and lifespan in complex organisms, including mammals.

• Korean Journal of Biological Psychiatry
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• v.22 no.2
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• pp.40-46
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• 2015

Neuroglial cells are fundamental for brain homeostasis and defense to intrinsic or extrinsic changes. Loss of their function and over-reactivity to stimuli contribute to the aging of brain. Alzheimer's disease (AD) could be caused by more dramatic response in neuroglia associated with various chemokines and cytokines. Neuroglia of the AD brain shares some phenotypes with aging neuroglia. In addition, neuroglial activation and neuroinflammation are commonly showed in neurodegeneration. Thus neuroglia would be a promising target for therapeutics of AD.