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Reversing aging: Is anti-aging protein GDF 1 1 a myth or a fairy tale?
As long as it is anticoagulant, don't bleed! The key lies in gene DNA-the ultimate information storage device? Who are you? Cell strain identity crisis! Robots can also be scientists? Tomorrow, will we still have jobs? Immortality is a dream that people from the emperor to the world have been striving for for for thousands of years. The most famous example is the first emperor of China, Qin Shihuang, who began to pursue immortality after he completed reunification at the age of 39, and sent people to the mountains and seas to look for a panacea many times. Today, 2200 years later, the biomedical field has not given up clarifying the factors and mechanisms of aging.

Because aging is an urgent problem for all countries in the world, muscular dystrophy, cardiovascular diseases and neurodegenerative diseases accompanying aging are a heavy burden for individuals and medical expenses. In recent years, scientists have discovered many genes and protein related to aging, the most notable of which is GDF 1 1 (growth differentiation factor 1 1), and found that it can improve the skeletal muscle function of aging rats, and was selected as one of the top ten scientific breakthroughs published in Science 20 14.

A milestone in anti-aging research-GDF11Improving Ventricular Hypertrophy 20 13 Amy Vargas and Li Canming's research team at Harvard Stem Cell Center, through the chronojunction; HP) connects the blood vessels of young mice and old mice, making them a part of blood circulation. To everyone's surprise, after four weeks of blood communication, the original myocardial hypertrophy of old mice has been improved. The experimental results seem to suggest that there is a rejuvenation factor in the blood of young rats? Therefore, through Western blot analysis, the research team found that there was a significant difference in the protein content of GDF 1 1 in the blood of young rats and old rats. The content of GDF 1 1 in the blood of old mice is relatively low, but after communicating with the blood of young mice, the GDF 1 1 in the blood of old mice. Therefore, the research team decided to separate the recombined GDF 1 1 (Rebbert GDF11; RGDF 1 1) was injected into old mice to test whether the effect similar to that in HP model could be obtained, so as to clarify the mechanism of improving the heart function of old mice with young mouse blood. Finally, thirty days after injection of RGDF 11(0.1mg/kg), the aged rats saw the effect of improving ventricular hypertrophy, so the researchers excitedly concluded that GDDF 1 1 has the potential to treat heart aging (note/kloc-)

GDF 1 1 helps muscle and nerve cells to regenerate for 20 14 years. Wager and Lee's research group published two articles about GDF 165438+ muscle degeneration accompanied by aging, because with the increase of age, the number of satellite cells responsible for repairing muscle tissue in the body decreased, and their activity also decreased. The researchers found that the aged rats injected with rGDF 1 1 could increase their running time and grip strength. The recovery of muscle function is presumably due to GDF 1 1, which can reduce the DNA damage of satellite cells in aging rats and improve the production of mitochondria. In another experiment, it was found that GDF 1 1 can improve the olfactory discrimination ability of aged rats by promoting vascular remodeling and neurogenesis. These studies seem to suggest that GDF 1 1 is a widely effective anti-aging factor, which can improve the function of heart, muscle and nerve cells. The research team evaluated GDF 1 1 as a potential anti-aging drug!

The voice of questioning GDF 1 1 appeared, but the voice of questioning GDF1/anti-aging began to appear. In the July 20 15 issue of Cell Metabolism, two articles questioned the activity of GDF 1 1. First, the research team from Novartis, a century-old pharmaceutical factory, openly challenged the anti-aging activity of GDF 1 1. Dr. David Glass, who led the research, said that the antibody of GDF 1 1 detected by Harvard team lacked specificity, and it could also identify GDF8, a myostatin, with a structural similarity of 89% to GDF 1 1. The results show that GDF 1 1 will increase with age, and SMAD2/3 will be phosphorylated, which will lead to the inability of myoblasts to differentiate and affect muscle regeneration (Note 4). The results of Novartis's research team are completely opposite to those of Harvard camp! Research by the University of Ottawa in Canada also pointed out that GDF 1 1 will bind with ACTRIIB and ALK-4/5 receptors during aging, thus inhibiting muscle regeneration (Note 5). These two reports are undoubtedly a blow to the anti-aging activity of GDF 1 1! It is followed by more questions about GDF 1 1. A study in Circulation Research pointed out that GDF 1 1 could not improve the phenomenon of ventricular hypertrophy (Note 6). 20 16, GlaxoSmithKline (GlaxoSmithKline; The research published by GSK) pharmaceutical company in Aging Cells also overturns the argument put forward by Harvard team that GDF 1 1 can activate skeletal muscle stem cells (note 7).

Response of Harvard Research Team: How did the Harvard team respond to these studies? Wagers and Lee's latest journal paper pointed out that the specificity of the anti-GDF 1 1 antibody used by Novartis team is the main reason for the inconsistent research results (Note 8), because this antibody can also recognize 25-kDa immunoglobulin light chain, but their previous antibody was GDF65438 with the size of 12.5-kDa. If we carefully observe the experimental data, we will find that the position of Novartis team in protein map 12.5-kDa is also GDF 1 1, which decreases with age. The experimental results of other teams may be due to the unstable recombinant protein and detection antibody of GDF 1 1 in the market, which leads different teams to draw different conclusions. Although GDF 1 1 is still controversial, the good news for the Harvard team is that the University of California (San Francisco) pointed out from the clinical report of 1899 patients with heart disease that when the patients' blood levels of GDF8 and 1 1 are high, the mortality rate will be low, and

Interestingly, Novartis Pharmaceutical Company challenged GDF 1 1 in a short time, and its motivation was unknown, because it was afraid that GDF 1 1 would affect their future business, because the monoclonal antibody Bimagrumab of Novartis for the treatment of inclusion myositis was in the second phase of clinical trials (note: in the latest industry development, It seems that the fact that young blood helps the aging rats to rejuvenate is also given to peter thiel (Ambrosia, co-founder of PayPal and Facebook investor, wants to invite 600 volunteers over the age of 35 to participate in the blood exchange experiment and accept the blood of healthy young people under the age of 25 to discuss the anti-aging effect, but only if the volunteers pay 8,000 US dollars (note 10).

GDF 1 1 needs more research to clarify its function. Although the function of GDF 1 1 is not clear, the detailed physiological mechanism needs to be developed by manufacturers and commercial recombinant GDF 1 1 protein, so that more researchers can clarify its function. But it is worth recalling that in the research history of GDF 1 1, we can see how an epoch-making discovery was debated and challenged by different research teams. Science is to discover the truth by arguing more and understanding more! And no matter what the final result of GDF 1 1 is, judging from the current industry trends, GDF 1 1 really ignited the fire of hope for anti-aging research!

Note *: Novartis Pharmaceutical Co., Ltd. announced that the clinical trial of Bimafumab Ⅱ B/Ⅲ failed in April 20 16.

References: 1. Loffredo et al. 20 13. Growth differentiation factor is a circulating factor that reverses age-related cardiac hypertrophy. Cell153,828-839. 2.Shiha et al, 20 14. Restoring the level of GDF 1 1 to reverse the age-related dysfunction of skeletal muscle in mice. Science 344,649-52. 3.Katsimpadi et al., 20 14. Effects of young systemic factors on the regeneration of blood vessels and nerves in the brain of aging mice. Science 344,630-4. 4. Eigermann et al., 20 15. GDF 1 1 inhibits skeletal muscle with age. Cell metabolism *** 22, 164- 174. 5. Bulun and Rudniki 20 15. GDF 1 1 and the mythical fountain of youth. Cell metabolism *** 22, 54-56. 6. Smith et al., 20 15. GDF 1 1 can't save the pathological hypertrophy related to aging. Circulation research117,905. 7. Hinken et al., 20 16. There is no evidence that GDF 1 1 is used as a regeneration agent for aging skeletal muscle satellite cells. Aging unit15,582-584. 8.Poggioli et al., 20 16. Cyclic growth differentiation factor 1 1/8 decreased with age. Circulation research 1 18, 29-37. 9. Olson et al., 20 15. The relationship between growth differentiation factor 1 1/8 (supposed anti-aging factor) and human cardiovascular disease and total mortality: * * Analysis of heart and soul and HUNT3 cohort. European Heart Journal 36 3426-34. 10. Joslin Kaiser 20 16. The anti-aging test of young blood raises questions. Science news, doi:10.1126/science.aag0716.

This article is reproduced from: GENEONLINE, the most professional media team in the field of genetics.

Subject: gene, gene detection, gene technology, anti-aging, aging