Wrong protein synthesis is an important reason to accelerate aging and shorten life!
The following is the Wrong protein synthesis is an important reason to accelerate aging and shorten life! recommended by recordtrend.com. And this article belongs to the classification: Life data.
Where are we from? Who are we? Where are we going?
We go to aging and death.
Aging is the inevitable outcome of most organisms. The study of aging, “why aging” and “can we keep aging” is one of the most profound and attractive studies in the history of science.
In the research of aging, there are dozens of theories put forward successively, some of which have become history and some are still shining. After you sing the theory of genetics, telomere theory, free radical theory and nutrition theory, we will appear on the stage. The nine aging markers are like the “nine dharmas” in the field of aging. They are implicated in each other and are difficult to win or lose. No one can prove that they are the real culprit of aging.
Note: Nine aging markers: genomic instability, telomere wear, epigenetic changes, loss of protein homeostasis, dystrophic induction, mitochondrial dysfunction, cell aging, stem cell failure and changes in intercellular communication
A recent study has made waves in this field, and the “error disaster theory” which has been silent for a long time has attracted people’s attention again.
“Error disaster theory” was put forward by chemist Leslie Orgel in 1963. He believes that the reason for aging lies in the error of RNA translation, which leads to the synthesis of defective proteins. More and more wrong proteins destroy the normal physiological function and eventually lead to aging.
At that time, there was no sufficient research evidence to support this theory. In recent years, there are also some evidences suggesting that the accumulation of wrong proteins will accelerate aging, including:
The long-lived star in rodents, the African naked mole with a life of up to 30 years, and the laboratory mouse 457 with a life of only 2-3 years have less missynthesized proteins in vivo;
After genetic modification of yeast, fruit fly and nematode to improve the accuracy of protein synthesis, their life span was prolonged by 23%.
Recently, Erik B ö ttger and his colleagues from the University of Zurich in Switzerland proved for the first time that the wrong protein synthesis can shorten the life span and accelerate aging of mammals. The study was published in science advances on March 2.
“This study fills a key gap, and we can finally be sure that missynthesized proteins are accelerators of aging.” Richard Morimoto, a molecular biologist at Northwestern University, commented.
In order to verify whether “mistakes in protein synthesis” can lead to mammalian aging, the researchers genetically modified the mice to obtain rps9 d95n heterozygous knock in mice, which have error prone ribosomes and produce more wrong protein in the process of translation. An example is that the length of protein produced by translation errors is too long, In rps9, the incidence of d95n mice was twice that of normal mice.
These rps9 d95n mice had little difference in appearance from ordinary mice when they were young and looked very healthy. However, at 9 months (equivalent to humans in their 30s), rps9 d95n mice began to show obvious premature aging, including hair loss, graying hair color, hunchback and chest deformation. The normal mice will not have one of these manifestations until they are 16 months old.
In terms of body composition, rps9 d95n mice began to lose weight and reduce the content of subcutaneous and visceral fat at 9 months, while ordinary mice did not lose weight until 18 months and humans were 65 years old.
In terms of motor function, compared with ordinary mice, rps9 d95n mice have slower walking speed, worse swimming ability and often sit still for a long time.
Moreover, rps9 d95n mice also showed premature anemia, lymphocytopenia in blood, monocyte proliferation and extramedullary hematopoiesis in spleen, which are the characteristics of mice that have reached the final stage of mouse birth. Anemia with unknown etiology is also a common symptom in elderly humans.
Rps9 d95n mice also showed molecular signs of premature aging. Compared with ordinary mice of the same age, they produced more free radicals, more serious oxidative damage, faster telomere length shortening, and epigenetic methylation during aging.
More importantly, the risk of early death of rps9 d95n mice was 7 times higher than that of ordinary mice. They began to die at 6.5 months (about 30 years old), and the death rate increased at 16 months. It can be seen that reducing protein can also shorten life span.
Figure note: survival curve of ordinary mice (gray) and rps9 d95n mice (pink)
All in all, this study proves that the wrong synthesis of protein will lead to accelerated aging and shortened life span, and the next urgent problem to be solved is – how does it lead to aging? Is wrong protein synthesis related to human aging diseases?
As the role of protein homeostasis in the aging process is gradually proved, researcher Erik B ö ttger proposed that “developing drugs to improve the accuracy of protein synthesis may become a new strategy to prevent aging”.
Reference source:
1.Glitchy protein production may hasten aging. https://www.science.org/content/article/glitchy-protein-production-may-hasten-aging
2.Shcherbakov D, Nigri M, Akbergenov R, Brilkova M, Mantovani M, Petit PI, Grimm A, Karol AA, Teo Y, Sanchón AC, Kumar Y, Eckert A, Thiam K, Seebeck P, Wolfer DP, Böttger EC. Premature aging in mice with error-prone protein synthesis. Sci Adv. 2022 Mar 4;8(9):eabl9051. doi: 10.1126/sciadv.abl9051. Epub 2022 Mar 2. PMID: 35235349.
3. López-Otín C, Blasco MA, Partridge L, Serrano M, Kroemer G. The hallmarks of aging. Cell. 2013 Jun 6;153(6):1194-217. doi: 10.1016/j.cell.2013.05.039. PMID: 23746838; PMCID: PMC3836174.
From: biological Valley
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