Release date: 2017-11-08
In order to delay aging, the ancients asked for immortality, alchemy took medicine, and now there are genetic editing, blood transfusion. Benqi’s cakes feel that it’s still a long way to live forever. It may take a few decades and hundreds of years for humans to study, or even a mirror.
Therefore, compared to these, this cake is still more concerned, how can we grow old with health and dignity? After thinking of old age, osteoarthritis may find the door, the action is no longer free; Alzheimer's disease may find the door, the memory is not good, life can not take care of themselves; heart disease may also find the door, physical strength can not work It’s been a little tired for a long time. It’s too painful to know that it’s too painful. I don’t know if you have such concerns.
In order to keep everyone healthy and old, a large number of scientists have been working hard. Among them, Professor Jan van Deursen of Mayo Clinic can be regarded as a leader. Now he and his team have developed a class of drugs called "senolytics" that can specifically remove the aging cells that cause the above-mentioned geriatric diseases, delay the onset of the disease or alleviate the symptoms of the disease. At present, they have conducted sufficient research in animal models, and clinical trials will soon be carried out. Nature has written a long news report for them [1].
Professor jan-van-deursen Jan van Deursen
In 2000, Professor Deursen was conducting a study on cancer, which he had been focusing on in the past, but there was something that made him puzzling. He and the team genetically engineered mice as usual. Transforming, "convenient" they develop cancer and conduct research. Unexpectedly, these mice did not have cancer, but they got a "strange disease". They had premature aging since 3 months, the hair began to become sparse, the subcutaneous fat was reduced, and the eyes also had cataracts. Etc. [2].
The curiosity of the scientists has plagued Professor Deursen for a long time. He began to look for the causes of premature aging in these mice. I didn't expect this to be 8 years. In 2008, he finally discovered that the original genetically modified mice were in vivo. The expression of two key genes involved in cellular senescence has increased. One of the genes, p16Ink4a, can promote cell senescence [3].
More than 50 years ago, scientists discovered that senescent cells stopped self-replication and division, but they refused to die. They just secreted some proteins like "zombies" to resist the arrival of death.
Early research suggests that this is the stress response that cells make when faced with certain stresses, especially genomic damage. Stopping the division prevents the proliferation of damaged or non-functional cells, thereby preventing the onset of tumors. In the same year that Professor Deursen found the cause of premature aging in mice, three research teams found that the accumulation of excessive senescent cells needs to be taken seriously because some of the cytokines, growth factors and proteases secreted by them affect neighboring cells, causing local inflammation. The body causes damage [4, 5, 6].
For young, healthy tissues and organisms, these secreted substances cause the "attention" of the immune system to be eliminated. However, as we age, aging cells accumulate in the body, and immune cells can no longer recognize and remove them, which is related to the occurrence of age-related diseases such as osteoarthritis.
Scientists have discovered that aging cells are widely found in tissues of humans, primates, and rodents, and in human age-related diseases such as osteoarthritis, pulmonary fibrosis, atherosclerosis, and Alzheimer's. Aging cells are found in the tissues of patients [7].
Professor Deursen suspects that if the aging cells in the body can be removed, it may delay aging.
To test this idea, in 2011, he collaborated with another professor of anti-aging research, Professor James Kirkland, to remove senescent cells expressing the p16Ink4a gene through a drug. They found that in the early life of mice, the elimination of senescent cells can delay the onset of aging symptoms in mice. In addition, even if the mouse has developed aging symptoms, timely removal of aging cells can also reverse the aging symptoms of mice to some extent. Their findings are published in the journal Nature [8].
Professor James James Kirkland
Can reverse aging? This is really a bad thing. According to this shocking discovery, Professor Deursen and Professor Kirkland have rushed to submit a research grant to the National Institutes of Health (NIH) to explore whether aging cells in normal mice can be eliminated. Delay the effects of aging.
However, this application has not been reviewed by the NIH expert panel. The explanation given by the NIH is that due to limited funding, the study is too innovative and too risky to support [9].
It’s true that “God closes a door for you and will open a window for youâ€. Just as Professor Deursen was unable to get the NIH funding, an entrepreneur named Nathaniel David was already on his way to work with him.
Ned Nathaniel David
Nathaniel David is a Ph.D. in Cell and Molecular Biology at the University of California at Berkeley. Before the “sparks†with Professor Deursen, five companies have been established, including three biotech companies and two energy companies.
On a three-hour flight, David read Professor Deursen's newly published paper. After reading it again, he felt that he had not finished it yet, and read it twice. When the plane landed, David called Professor Deursen's phone and Within 72 hours, he persuaded Professor Deursen to interview and form an anti-aging company. In David's opinion, Professor Deursen's idea of ​​removing aging cells to delay aging is simply "simpler and beautiful, almost poetic!"[1]
The reason why David wants to form an anti-aging company so quickly is that he appreciates and is convinced that the innovation of this discovery is a bit "selfish."
Because his father suffered from early-onset osteoarthritis in his teens, it was also a premature aging disease. The old man was already in bed and could not move. Affected by heredity, David itself also developed early symptoms of degenerative disc disease. If they can develop anti-aging drugs, then David does not have to endure the pain of his father [10].
Next, David invited another expert in the field of anti-aging, Professor Judith Campisi of the Buck Institute on Aging, and she was also one of the three teams that discovered the accumulation of aging cells that could trigger inflammation in 2008. . Together with Professor Deursen, the trio set up an anti-aging company called "Unity Biotechnology" in San Francisco.
Professor CampisiJudith Campisi
Later, several scientists began the "tough road". Because the aging cells in different tissues were found to be slightly different, the cytokines secreted by them, the extracellular proteins expressed and the ways to resist death were different. Therefore, it is possible that each drug can only work for specific aging cells. For different geriatric diseases, multiple types of drugs may be needed, which is why we call senolytics "a class of drugs" at the beginning.
In 2015, Professor Kirkland found the first “senolytics†drug to eradicate aging cells, the FDA-approved dasatinib for cancer treatment. Dasatinib can effectively remove aging human fat cells. In addition, a compound extracted from plants, quercetin, can eliminate aging endothelial cells. Premature aging mice are treated with dasatinib and quercetin regularly, and the elimination of senescent cells can prolong the disease-free lifespan of the mice and delay the onset of some age-related diseases, such as decreased exercise capacity [11]. .
In February 2016, Professor Deursen published a study in Nature magazine [12]. This study is also very powerful. By removing senescent cells, they have extended the average lifespan of normal aging mice by about 1/4 (17). %-35%)! It also slows down organ degradation associated with aging, such as the kidneys and heart, without significant side effects.
In August of the same year, Professor Deursen collaborated with Professor Campisi to publish a study in another authoritative journal, Science, using "senolytics" drugs to remove senescent cells from mice, for mice in the early stages of atherosclerosis. In fact, it can completely remove its early lesions, and even in the advanced stage, it can greatly reduce atherosclerotic plaques [13].
This year, their search for new breakthroughs has not stopped. In the mouse model of osteoarthritis and osteoporosis, “senolytics†drugs clear aging cells, prevent or even reverse the disease, providing new chondrocyte production. Conditions, the study was published in the journal Nature Medicine in April and September [14,15]. Another study published by Professor Campisi, published in the journal Cell, showed that after using a peptide to remove senescent cells, the kidney function of the mice is improved and the hair is restored to youthful luster [16].
To date, scientists have identified 14 "senolytics" drugs, including small molecules, antibodies and peptides. Unity Biotechnology has created a large archive detailing which aging cells correspond to which disease, and which drugs can remove information such as aging cells.
It is worth mentioning that it is not necessary to kill all aging cells in tissues for the treatment of aging-related diseases. Mouse studies have shown that killing most cells is enough to make a difference. Therefore, you only need to clear the aging cells regularly, such as once a year. This means that the "senolytics" drug has a shorter medication period, and the "running and running" treatment strategy can avoid many side effects.
In addition, "senolytics" drugs only affect existing senescent cells and do not interfere with the formation of such cells, which means that the original tumor suppressor function of senescent cells can still be retained.
Of course, "senolytics" drugs can really be used in human anti-aging and there is still a long way to go, as Professor Deursen said: "Resolving the mystery of aging is an eternal topic for human beings. Only by truly understanding the true appearance of the old can we Intervene in aging in a sensible way."[1]
Reference materials:
[1] https://
[2] Baker DJ, Jeganathan KB, Cameron JD, et al. BubR1 insufficiency causes early onset of aging-associated phenotypes and infertility in mice [J]. Nature genetics, 2004, 36(7): 744-749.
[3] Baker DJ, Perez-Terzic C, Jin F, et al. Opposing roles for p16Ink4a and p19Arf in senescence and ageing caused by BubR1 insufficiency[J]. Nature cell biology, 2008, 10(7): 825-836.
[4] Coppé JP, Patil CK, Rodier F, et al. Senescence-associated secretory phenotypes reveal cell-nonautonomous functions of oncogenic RAS and the p53 tumor suppressor [J]. PLoS biology, 2008, 6(12): e301.
[5] Kuilman T, Michaloglou C, Vredeveld LCW, et al. Oncogene-induced senescence relayed by an interleukin-dependent inflammatory network [J]. Cell, 2008, 133(6): 1019-1031.
[6] Acosta JC, O'Loghlen A, Banito A, et al. Chemokine signaling via the CXCR2 receptor reinforces senescence [J]. Cell, 2008, 133(6): 1006-1018.
[7] Van Deursen J M. The role of senescent cells in ageing [J]. Nature, 2014, 509(7501): 439-446.
[8] Baker DJ, Wijshake T, Tchkonia T, et al. Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders[J]. Nature, 2011, 479(7372): 232-236.
[9]http://
[10] https://qz.com/878446/unity-biotechnology-cure-for-aging/
[11] Zhu Y, Tchkonia T, Pirtskhalava T, et al. The Achilles' heel of senescent cells: from transcriptome to senolytic drugs [J]. Aging cell, 2015, 14(4): 644-658.
[12] Baker DJ, Childs BG, Durik M, et al. Naturally occurring p16Ink4a-positive cells shorten healthy lifespan[J]. Nature, 2016, 530(7589): 184-189.
[13] Childs, BG, et al., Senescent intimal foam cells are deleterious at all stages of atherosclerosis. Science, 2016. 354(6311): p. 472-477.
[14] Jeon OH, Kim C, Laberge RM, et al. Local clearance of senescent cells attenuates the development of post-traumatic osteoarthritis and creates a pro-regenerative environment[J]. Nature Medicine, 2017, 23(6): 775 -781.
[15] Farr JN, Xu M, Weivoda MM, et al. Targeting cellular senescence prevention age-related bone loss in mice [J]. Nature Medicine, 2017, 23(9): 1072-1079.
[16] Baar MP, Brandt RMC, Putavet DA, et al. Targeted apoptosis of senescent cells restores tissue homeostasis in response to chemotoxicity and aging[J]. Cell, 2017, 169(1): 132-147. e16
Source: Singularity Network
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