Researchers have shown that tweaking the tiny inner parts of a cell could prevent the damage caused due to aging.
The results of this new breakthrough study were published in the latest issue of the journal Genes and Development. This study titled, “Nuclear pore density controls heterochromatin reorganization during senescence,” was backed by the Medical Research Council and by Cancer Research UK.
Image Credit: Syda Productions / Shutterstock
Researchers have shown how the process of cell aging or senescence could be stopped or prevented. This finding could have a major impact on age related diseases such as cancers and diabetes, explain the researchers. They add that as the cell ages, there is a cessation of cell division. This process can be utilized to benefit wound healing or prevent excess cell division as seen with cancers. Senescence on the other hand could lead to decline in cell health and tissue damage.
The researchers from the Medical Research Council's Human Genetics Unit and the Cancer Research UK Edinburgh Centre at the University of Edinburgh targeted the process of senescence. They explain that senescence can trigger a process called the senescence-associated secretory phenotype (SASP). SASP is basically a series of processes that lead to chemical signals that cause cell damage due to inflammation. The researchers found that if they could modulate the nuclear pores or gateways of the nucleus of the cell, SASP triggers could be stopped. For SASP to come into action, DNA too has to be altered, they add. If these steps could be modulated, senescence and its effects could be controlled they explain.
Study leader, Professor Wendy Bickmore, Director of the Human Genetics Unit at the University of Edinburgh's Medical Research Council Institute of Genetics and Molecular Medicine, in a statement said, “These findings provide us with a much clearer understanding of how senescence causes cell damage. Whilst we are some way from being able to halt the damage caused by the ageing process, we hope that this advance will open up avenues to explore how we might slow some of the harm that stems from senescence. This could be of relevance to the many conditions that tend to affect us as we grow older.”
Dr Lindsay Wilson, Programme Manager for Genetics, Epigenetics and Genomics at the Medical Research Council, also said that this study shows “how cells respond to damage and stress”. She said, “Senescence is an essential self-defence mechanism but at times, can also be harmful. Professor Bickmore's work suggests ways in which scientists of the future might target these harmful effects, for example in age-related diseases.”
Dr Masashi Narita from the Cancer Research UK Cambridge Institute also said that thus was “an extremely important area in biology”. She said, “This work is still a long way off benefits for people, but provides helpful clues to how we might be able to manipulate this process in the future.”
Source: http://genesdev.cshlp.org/content/33/3-4/144