In a new study, researchers found that certain genes that regulate splicing factors play a key role in the aging process.
These genes are a group of proteins in our body that tell our genes how to behave.
Significantly, the team found that disrupting these genetic processes could reverse signs of aging in cells.
The Research has shed new light on genetic processes that may one day lead to the development of therapies that can slow, or even reverse, how our cells age.
The study was led by the University of Exeter. It was conducted in human cells in laboratories.
Aged, or senescent, cells are thought to represent a driver of the aging process and other groups have shown that if such cells are removed in animal models, many features of aging can be corrected.
This new work from the Exeter team found that stopping the activity of the pathways ERK and AKT, which communicate signals from outside the cell to the genes, reduced the number of senescent cells in in cultures grown in the laboratory.
Furthermore, the researchers found the same effects from knocking out the activity of just two genes controlled by these pathways—FOX01 and ETV6.
The team is really excited by the discovery that disrupting targeted genetic processes can bring about at least a partial reversal of key elements of the aging process in human cells.
This suggests that it is possible to design therapies that could keep us healthier as we age.
The ultimate goal is to help people avoid some of the diseases partially caused by aging cells, such as dementia and cancer.
The ERK and AKT pathways are repeatedly activated throughout life, through aspects of aging including DNA damage and the chronic inflammation of aging.
The research suggests that this activation may hinder the activity of splicing factors that tell genes how to behave.
This, in turn, could lead to a build-up of senescent cells—those which have deteriorated or stopped dividing as they age.
To stop the activity of the ERK and AKT pathways, the study used inhibitors which are already used as cancer drugs in clinics.
When the pathways were disrupted, the team observed an increase in splicing factors, meaning better communication between protein and genes.
They also noted a reduction in the number of senescent cells.
They saw a reversal of many of the features of senescent cells that have been linked to the aging process, leading to a rejuvenation of cells.
The researchers suggest that this study is part of a fast-evolving body of work into how we age.
It’s still early days and they need to understand far more about the complex relationships of how our cells and genetic processes influence aging.
But it’s an exciting contribution to how scientists may one day be able to influence healthier aging.
Professor Lorna Harries of the University of Exeter Medical School led the research. Dr. Eva Latorre of the University of Exeter Medical School carried out the research.
The study is published in the FASEB journal.
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Source: FASEB.
