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New Molecule Identified for Eliminating Senescent Cells and Delaying Tissue Aging

Scientists from the UOC and the University of Leicester have made a groundbreaking discovery in the field of aging research. They have identified a new molecule, CUDC-907, that has the potential to selectively destroy aging, non-functional cells known as senescent cells, without affecting healthy ones. This discovery could have significant implications for delaying tissue aging, improving life quality, and extending longevity.

As the body ages, cells start to accumulate and stop functioning properly, leading to the aging of tissues. The joint research effort by the UOC and the University of Leicester has found a molecule that can eliminate these old cells without impacting healthy ones. This finding opens up possibilities for delaying tissue aging and ultimately improving the quality of life and life expectancy in humans.

The results of this research have been published in the journal Aging in an open-access format. The experiments conducted so far have been in vitro, using cells in a controlled laboratory environment. The next step is to test the molecule in animal models to further evaluate its effectiveness.

Throughout a person’s life, cells undergo various types of stress, such as solar radiation, which can lead to the accumulation of mutations. The body has defense mechanisms to prevent the development of tumors. Cells either undergo apoptosis, a process of self-destruction, or become senescent, a state in which they no longer function properly but remain alive. Senescent cells also produce products that replicate this state in surrounding healthy cells.

While the immune system can eliminate these senescent cells and clean up tissues when the organism is young, it becomes less effective as people age. This leads to the accumulation of senescent cells in tissues, impairing their function and contributing to the aging process.

Previous studies in animals have shown that drugs called senolytics, which can eliminate these old cells, can improve life expectancy and quality of life. The researchers, led by Professor Salvador Macip, have identified a molecule called CUDC-907 that efficiently and specifically destroys old cells with minimal side effects on healthy cells.

CUDC-907 is also being investigated for its potential anti-cancer effects. In cancer treatment, the drug inhibits two cell communication pathways, one of which was previously unknown and discovered by Macip’s team. It targets cells that are extensively damaged by chemotherapy or radiotherapy but do not die, instead becoming senescent and potentially leading to the recurrence of tumors. By administering CUDC-907 alongside traditional cancer treatments, the researchers hope to reduce cancer relapses.

The researchers have found that CUDC-907 eliminates a specific type of senescent cell with limited side effects in different models of human cancer cells. The next step is to test the molecule in animal models, and if successful, move on to human trials. The researchers also believe that CUDC-907 could be applied in diseases where the accumulation of senescent cells plays a role, such as Alzheimer’s disease.

The potential of CUDC-907 is significant, as it could not only delay tissue aging but also have a dual effect of combating cancer and targeting old cells that contribute to its recurrence. Further research and testing will determine the full extent of its capabilities and its potential applications in improving human health and longevity.

Reference: “Characterization of the HDAC/PI3K inhibitor CUDC-907 as a novel senolytic” by Fares Al-Mansour, Abdullah Alraddadi, Buwei He, Anes Saleh, Marta Poblocka, Wael Alzahrani, Shaun Cowley, and Salvador Macip, 28 March 2023, Aging. DOI: 10.18632/aging.204616
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How does the molecule CUDC-907 selectively destroy aging, non-functional cells while leaving healthy cells unaffected?

Scientists from the UOC and the University of Leicester have made a significant breakthrough in the field of aging research. Through their joint efforts, they have discovered a molecule called CUDC-907 that can selectively destroy aging, non-functional cells known as senescent cells, while leaving healthy cells unaffected. This discovery has the potential to delay tissue aging, improve quality of life, and extend longevity.

As the body ages, cells begin to accumulate and lose their proper functioning, causing tissues to age. However, the researchers have found that CUDC-907 can eliminate these old cells without harming the healthy ones. This finding opens up new possibilities for slowing down tissue aging and ultimately enhancing the well-being and life expectancy of individuals.

The results of this groundbreaking research have been published in the open-access journal Aging. The experiments conducted so far have involved studying cells in a controlled laboratory setting. The next step is to evaluate the molecule’s effectiveness by testing it on animal models.

Throughout a person’s lifetime, cells undergo various types of stress, such as solar radiation, which can result in the accumulation of mutations. The body has defense mechanisms to prevent tumor development, either causing cells to undergo apoptosis (self-destruction) or enter a senescent state in which they no longer function properly but remain alive. Moreover, senescent cells also release products that replicate this state in surrounding healthy cells.

While the immune system can remove senescent cells and restore tissue health when an individual is young, it becomes less efficient as people age. This leads to the buildup of senescent cells in tissues, hindering their function and contributing to the aging process.

1 thought on “New Molecule Identified for Eliminating Senescent Cells and Delaying Tissue Aging”

  1. This new breakthrough in identifying a molecule to eliminate senescent cells and delay tissue aging is truly promising! It is exciting to think about the potential implications this discovery may have on extending healthy lifespans. Looking forward to seeing further research in this area.

    Reply

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