Variation in ageing cells may determine your risk of developing age-related diseases, new study suggests
A group of researchers at Kumamoto University, Japan, said that cellular senescence, the process of arresting cell division, may be used to improve health, longevity and reduce the risk of developing age-related diseases
Better healthcare facilities, improvement in education, sanitisation and housing has significantly increased human life expectancy over the past few decades. However, the world is now facing a quickly ageing population, especially in developed countries where better facilities are available and people tend to live longer even with chronic conditions. Since the older population is likely to increase in the coming years, experts suggest that it is important to find ways to maintain healthier life spans.
Now, a group of researchers at Kumamoto University, Japan, say that cellular senescence, the process of arresting cell division, may be used to improve health, longevity and reduce the risk of developing age-related diseases.
The findings of the study are published in the journal Trends in Cell Biology.
Cellular senescence is a process in which the body cells stop dividing and undergo some phenotypic alterations such as changes in chromatin (consists of DNA and proteins), proteins released by the cells and activation of tumour suppressors (proteins that suppress tumour growth).
This process can occur due to ageing or on exposure to stressors like radiation, drugs or UV light. Cellular senescence can be good, like when it stops the spread of cancerous cells. However, it has previously been shown that senescent cells secrete various proteins that act on the surrounding cells and trigger inflammation. This is what causes age-related diseases.
Experts suggest that studying cellular senescence may help control all the side effects of the process. In fact, studies in mice have shown that removing senescent cells may suppress whole-body ageing.
The various stages
The researchers at Kumamoto University are studying the activity of about 25,000 protein-coding human genes involved in the various processes of health and ageing in the body.
So far, the team has screened for a wide range of factors involved in human fibroblast ageing and has found that proteins called SETD8 methyltransferase and NSD2 methyltransferase can reverse cellular senescence. However, so far, we don’t know of any biomarkers that can help us identify senescent cells.
To study the whole process of cellular senescence, the researchers viewed the process over a span of time and noted that cells go through four phases during the process of senescence. These include:
- Initiation - where cell proliferation stops
- Early - where inflammation reduction happens due to an increase in anti-inflammatory cytokines
- Full - where inflammation increases (due to an increase in pro-inflammatory cytokines) along with metabolism
- Late - where both inflammation and metabolism decrease.
Studying each stage on the molecular level, the researchers noted that the on and off of the various genes and changes in metabolism occur in a coordinated manner throughout the process of senescence.
Though more studies are still needed to better understand how the process works, the authors indicated that the study sheds light on the previously unknown mechanisms of cellular senescence.
In a news release by the Kumamoto University, professor Mitsuyoshi Nakao, the corresponding author of the study, said, “We hope that our work will provide an opportunity for the scientific community to consider a new understanding of the mechanisms of cellular senescence and body ageing," He added, "We believe that phenotypic variation in cellular senescence can lead to new methods to promote healthy longevity and the control and prevention of age-related diseases."
For more information, read our article on Inflammatory disease.
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