Reversing the human aging process is no longer illogical.
By using 3 out of 4 special proteins to convert differentiated cells into pluripotent stem cells (iPSCs), the research team led by Professor Sinclair (Harvard Medical University, USA) succeeded. in repairing damaged retinas in aging mice, helping to improve vision. After that, the group continued to research on muscle cells and brain cells in mice, progressing to applying research on the entire mouse body. In a latest study published earlier this year, the Sinclair team discovered another major cause of aging is the loss of epigenetic information due to DNA breaks, and succeeded in restoring it. epigenetic information was lost, reversing the aging process in mice. If you have interest in anti-aging products, you can also refer to this website for more information.
The first important milestones in aging research
The experiment of the research group led by Professor Sinclair (referred to as the Sinclair group) is a continuation of the success of Professor Shinya Yamanaka’s previous research in reestablishing pluripotent stem cells from human skin cells. From there, pluripotent stem cells can differentiate into any other cell type in the body, and the four main factors in the stem cell regeneration cycle are Oct4, Sox2, Klf4 and c-Myc (OSKM). Professor Shinya Yamanaka’s research was awarded the 2012 Nobel Prize (along with Professor John B. Gurdon). Afterwards, Professor Shinya Yamanaka’s name was given to his own discoveries: “Yamanaka factors — Yamanaka factors”. However, human cells, after converting back into stem cells through Yamanaka factors, lost the ability to “recognize” themselves. In other words, the cells that “forget” themselves are cells from the blood, heart cells or skin cells, as if those cells have been regenerated and at the same time forgotten their “previous lives”.
After the Yamanaka study, another study published in the journal Cell in 2016 showed that, in a mouse model that had been genetically modified to promote aging, when Yamanaka factors were introduced into the mouse body in A short period of time can erase the signs of aging, even prolonging life without losing the cell’s ability to recognize. However, in some cases, “rejuvenated” mice are at risk of developing cancer.
With a safer alternative, the Sinclair group selected three of the four Yamanaka factors including Oct4, Sox2, and Klf4 (OSK) to introduce into a harmless virus (dual adeno-associated virus system — roughly translated: vector system dual Adeno virus), then injected into the vitreous body, just behind the damaged corneal rim of the old mouse eye. After injecting the virus, the genes will be activated with the antibiotic Doxycycline orally. The results were amazing, the damaged nerve cells in the mouse eyes were “rejuvenated”, even growing new axons connecting from the eye to the brain. The Sinclair group suggests that the three OSK factors can restore youthful DNA methylation patterns and transcriptomes, promote axonal regeneration after injury, and reverse vision loss in a mouse model of glaucoma. and old mice.
Limitations of the study
Despite significant advances, the Sinclair team’s research also has limitations. The first point is that despite reversing DNA methylation in neurons as well as RNA sequencing, the team did not show any phenotypic changes. Although the research team provided evidence that the mouse model promoted aging by assessing activity and cognition as well as immunohistochemistry of relevant tissues, it did not provide evidence to evaluate the effects of aging. price when reversing the aging process. For example, life expectancy, changes in musculature and cognition, or changes in cell or tissue characteristics have been reported in previous studies. In addition, more information is needed about other cell types besides neurons, and whether OSK factors regenerate differently when comparing different cell types or tissues. For example, do liver or kidney cells exposed to OSK undergo the same epigenetic changes? Identifying site-specific epigenetic changes in different tissue types is of great significance for better understanding the context of cellular rejuvenation.
Besides DSB, there are other forms of DNA damage such as single strand breaks, chromosome rearrangements, and oxidative base damage that also cause aging through epigenetic changes. Other DNA will provide a more multidimensional perspective on the cellular aging process.
Sinclair’s team’s research marks an important milestone in reversing the aging cycle, promising to bring many benefits to humanity. Currently, we can expect the research to be applied to higher animal models or further to human applications. Most importantly, it lays the foundation for future treatment research on age-related diseases such as cancer or blood pressure
