Aging is a natural process. With the growth of age, all people will gradually grow old, which seems to be an unchangeable natural law. In recent years, with the acceleration of the global aging process, countries around the world have launched a wave of anti-aging research, and various anti-aging drugs and therapies have also been found, such as nicotinamide, metformin and senolytics.
Previous studies have shown that the aging process of life is partly due to the development of aging cells. These aging cells have been unable to function, but they have not died naturally. At this time, these senescent cells will continue to produce many pro-inflammatory and tissue remodeling molecules and be poisoned by other cells. In addition, scientists found through transcriptome analysis that cancer cells, like bad old cells, can increase the expression of "Pro survival network" to help them resist apoptosis or programmed cell death.
Recently, researchers from Juntendo University in Japan published a research paper in the journal nature aging, entitled: senolytic infection improves normal and pathological age-related phenotypes and increases lifespan in progeroid mice This study identified a target of senolytic therapy: glycoprotein non metastatic melanoma protein B (gpnmb).
Gpnmb is enriched in senescent cells.
Gpnmb antibody was developed and used as a vaccine to improve the aging symptoms of mice and prolong the life span of mice, especially male mice. Selective removal of senescent cells can improve normal and senescence related changes in mice. However, most drugs that clear senescent cells inhibit the anti apoptotic pathway, which may increase the off target effect of normal tissues. Therefore, it is necessary to identify specific targets for hemolytic therapy.
In this latest study, the research team identified glycoprotein non metastatic melanoma protein B (gpnmb) as the molecular target of senolytic treatment. Gpnmb is a transmembrane protein. Transcriptome data analysis of aging vascular endothelial cells showed that gpnmb was enriched on the surface of aging cells. Gpnmb is also upregulated in vascular endothelial cells and / or leukocytes of human patients and atherosclerotic mice.
This study shows that gpnmb is an important regulator of adipogenesis. Gpnmb increases fatty acid synthesis in white adipose tissue, exacerbating diet induced obesity and insulin resistance. Neutralizing antibody blocking gpnmb can improve diet induced obesity and insulin sensitivity. Therefore, inhibiting gpnmb is a potential treatment for obesity and diabetes.
This new study in nature aging confirmed that knockout of gpnmb can reduce metabolic abnormalities and atherosclerosis in mice on a high-fat diet and improve aging status.
The research group developed an antibody against gpnmb protein and used it as a vaccine. After injection, the antibody produced by the vaccine only binds to gpnmb protein on the surface of senescent cells, thereby labeling senescent cells and inducing antibody dependent cell-mediated cytotoxicity (ADCC) to kill these senescent cells. Next, the team validated the vaccine in atherosclerosis, a disease caused by the accumulation of aging cells, and aging mouse models.
The experimental results showed that the vaccine could reduce the number of aging cells in the sclerotic arteries and alleviate the aging related symptoms such as weakness of aging mice. In addition, this senolytic vaccine can prolong the life span of mice (average 20%), especially that of male mice. It is suggested that this anti-aging antigen senolytic vaccine can be used as a new senolytic therapy.
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