Molecular mechanism of aging and therapeutic advances through targeting glycative and oxidative stress

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About this Research Topic

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Background

Aging is an unavoidable and irreversible biological phenomenon for all living organisms. It is caused by structural and functional loss of different proteins (for example telomerase), DNA, and cells which can lead to the functional loss of organs and subsequent bodily function. This loss can also cause numerous age-related diseases including allergies, arthritis, asthma, autoimmune diseases, inflammatory diseases, diabetes, kidney failure, heart failure, Alzheimer's, Huntington's and Parkinson's disease. Furthermore, the uncontrolled growth of cells can ultimately lead to cancer. While these tend to be age-related diseases, they are also still observed, to a lesser extent, in the younger population. Aging is slow taking decades to cause any visible signs and symptoms making it difficult to conduct age-related research in humans due to longer lifespan, difficulty to control lifestyle and food habits.

Aging prompts dramatic incurable changes in most of the body, organs, and skin. Although the causes of aging are still unknown and requires more extensive research, some causes have been reported e.g. increased glycative stress observed with age. Non-enzymatic glycation causes structural and functional changes of cellular building-blocks and triggers detrimental effects on health. Elevation of the formation of advanced glycation end products and their accumulation has been observed in patients with osteoporosis, osteoarthritis, diabetes, and retinal dysfunction. Glycative stress is reported to induce oxidative stress and ER stress and thereby cause cell death or cell dysfunction in different cell types including immune cells, neuronal cells, bone cells etc.

Another noticeable observation is the interference of enzymatic glycosylation by glycation. Enzymatic glycosylation is very important for protein structure and function. Glycation may interfere with enzymatic glycosylation by targeting either the predetermined region of the protein that is supposed to be glycosylated or the enzymes themselves (glycosyltransferases). Currently, there is no therapeutic approach to reverse the effects of glycation. Therefore, glycation prevention is a prerequisite to slow down aging. Understanding the mechanism of aging through glycative stress and oxidative stress could lead us to find methods of treatment and prevention of aging and age-related diseases.

In this Research Topic we welcome original research manuscripts and reviews that include, but are not limited to, the following themes:

- Reviews or hypothesizes focusing on the structural and functional changes upon aging of proteins, cell or animal models.

- Articles that aim to further clarify molecular mechanisms in order to establish a new research model of aging.

- Factors that alter cell death and differentiation over time and which could be a potential target in age-related diseases.

- Technological advances for the early diagnosis of aging or disease.

- The accelerating or decelerating effect of hormones, lifestyle, food habits, and exercise on aging.

- The impact of obesity on the aging process.

- The role of microbiome and their products on aging, reducing, or accelerating glycative stress, oxidative stress, insulin resistance, inflammation, telomere shortening.

- Natural or chemical substances that possess a preventive effect on the aging process that could be beneficial for health. Mechanistic studies behind their beneficial effects are important.

Research Topic Research topic image

Keywords: Aging, cell death and differentiation, structural and functional change of proteins, oxidative stress, glycative stress, bone diseases, neuronal disorders, microbiome.

Important note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.

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