More true 丨 Chinese scientists decipher the code of human aging, "old without aging" can be achieved?

True points:

1. The study did find a gene, KAT7, which is associated with aging, but only experimented with mice, and the media's interpretation of the findings was too fleshed out.

2. Humans and mice are very different, KAT7 also has other functions, in the end can you intervene in the function of KAT7 to delay human aging? More research is needed.

3. The "old and not fading, old and disease-free" mentioned in the news is only a goal and ideal expressed by the researchers in the interview, from the ideal to the reality, there is still a long way to go.

Verifier: A section of Ginger 丨 Associate Professor of Research in the Department of Pathology and Experimental Medicine, University of Pennsylvania School of Medicine

Recently, there are news reports that Chinese scientists have found a molecular switch to "keep cells young", which can slow down the rhythm of cell aging by resetting the epigenetic clock of aging, and achieve old age without aging, old and disease-free!

What's going on here?

First, is the study of the molecular switch of "keeping the cell young" true?

The research mentioned in the relevant reports is true, and the paper was published this year in the journal Science 丨 Translational Medicine.

In the study, researchers at the Institute of Zoology of the Chinese Academy of Sciences used human mesenchymal precursor cells (hMPCs) that accelerate aging due to genetic mutations, and through crispr gene clipping, they found a gene associated with aging: KAT7.

KAT7 is a histone acetyltransferase that regulates gene transcription. To verify the function of KAT7, the researchers used a lentiviral vector to directly perform gene editing on mice with physiological aging and a type of progeria, and found that the lifespan of the mice was extended, and the aging of liver cells and livers was alleviated.

Second, "old but not aging, old and disease-free", can it be realized?

Although the study is true, the media's interpretation of the results is too fleshed out.

In the news report, it was mentioned that "after partial inactivation of the gene in the liver of elderly mice, 81% of the mice can be more than 130 weeks old, which is about the same as the human age of 80", this expression is actually not accurate.

The 130-week age of mice translates into human lifespan, how old is it? Under normal circumstances, wild mice live for about one year, but mice bred in the laboratory can live to about 2 years because of better conditions. Therefore, changing the living environment and improving sanitary conditions can greatly extend life expectancy, which is also the same as the human situation. If the natural lifespan is converted, the nine days of the mouse is equivalent to one year for humans, then the mouse 130 weeks is already 101 years old (not 80 years old) of the human.

To figure out how much longer life expectancy will be achieved after knocking out the KAT7 gene, it is necessary to compare the lifespan of gene-edited mice and normal mice. The data from this study shows that the median lifespan of naturally aging mice is about 105 weeks (that is, half of the mice have a longer lifespan of 105 weeks), while the mice knocked out OFT7 exceed 140 weeks, which is equivalent to an increase in lifespan of more than 30%!

If human life expectancy can be increased by 30% as the test results, it will be 90 to 100 years old!

It should be pointed out that although the results of this study are good and the paper has been published, it is only experimented with mice, which does not mean that the same results will be obtained in humans. There have been many other studies on aging before, such as resveratrol, which can extend the lifespan of mice by 31%, but it has not yet been realized in humans.

The "old and not aging, old and disease-free" mentioned in the news is only a goal and ideal expressed by the researchers in the interview, not the reality that is about to happen! There is still a long way to go from ideal to reality.

Third, what is the obstacle between the ideal and reality?

Why is it that the 30% increase in lifespan in mice is not easy to do in humans?

A very simple answer: because humans are not mice.

Although humans and mice are mammals, there is still a big difference in genes. Not only that, but there are not many differences between individual mice used for experiments, and there are many differences between human individuals, and the causes of aging and disease will be diverse. For these reasons, it is impossible to fully prove the therapeutic function of a drug through animal experiments, and it must be verified by clinical trials in humans.

Specific to KAT7, while research suggests it is a gene that causes aging, it is not the only gene that does this. In addition, KAT7 also has other functions, and studies have shown that KAT7 plays a key role in the regulation of immune T cell development, and if THERE is no KAT7, immune cells will be greatly reduced.

If this gene is knocked out in humans, will it have side effects or cause the immune system to function poorly? This requires more research to figure it out.

Obviously, even if the future can be delayed by interfering with the function of KAT7, it is unlikely to engage in "one-size-fits-all" and completely remove the KAT7 gene, which can only be targeted for certain cells, or reduce the activity of KAT7 in a specific period through targeted drugs.

Scientific research is not easy, and scientists need to continue to work hard.

This article was edited by: courtneyli

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