‘Hope for Healthy Longevity’: Study Discovers Trigger for Cell Aging

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Previously, mechanical damage to the cell membrane was believed to trigger either cell recovery or death. A new study shows a third outcome: cell aging.

Keiko Kono hopes to see a future where people are essentially healthy until the day they die.

She believes her recent research—which shows that damage to the cell membrane promotes cell aging—could serve as a blueprint for scientists worldwide to find a way to do this.

Her article was recently published in Nature Aging.

Membrane Damage Switches Cell Fate

“I discovered a new trigger of cell aging,” Ms. Kono, an assistant professor of membranology at Okinawa Institute of Science and Technology (OIST), told The Epoch Times, describing the culmination of her 10 years of research. Ms. Kono hopes the discovery will prompt additional research and future drugs that help prevent membrane damage.

Human cells are surrounded by a fragile 5-nanometer-thick membrane comparable to one-twentieth of a soap bubble, Ms. Kono said. Consequently, cells are easily damaged by a multitude of internal and external stressors. To protect the body from disease and to stay alive, cells are equipped with repair pathways to mend membrane damage to a certain degree.

Until now, mechanical damage to the cell membrane was believed to trigger two simple cellular outcomes: recovery or death. In Ms. Kono’s study, researchers uncovered a third outcome—cellular senescence, or cell aging.

“Initially, I wasn’t aiming to address the question of aging or anything. I was just wanting to answer a very fundamental question: how our cells can repair membrane damage,” Ms. Kono said. “We ended up discovering that cell membrane damage, in a sense, switches cell fate.”

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Ms. Kono and her colleagues used budding yeast and normal human fibroblasts, or fibrous cellular material that supports and connects other tissues or organs.

Ms. Kono said the key to determining cell fate is the extent of damage and subsequent calcium ion influx, which may control cell excitability, neurotransmitter release, or gene transcription.

Unlike cancer cells, which divide unlimitedly, noncancerous normal cells have a limited capacity for cell division: around 50 times before division is irreversibly stopped, and the cells enter a state known as cellular senescence. Senescent cells are still metabolically active—or conducting chemical processes necessary to remain alive—but unlike young and healthy cells, they produce proteins that upregulate immune responses in both nearby tissues and distant organs.

Cellular senescence is involved in processes everywhere in the body, including wound repair, cell division, and cell growth. But prolonged senescence can be maladaptive and lead to cancer, DNA damage, changes in how genes work, and age-related diseases.

Researchers have long believed that various stresses induce cellular senescence via the activation of DNA damage response, Ms. Kono said. However, her study revealed that cell membrane damage induces cellular senescence via a different mechanism. These findings may contribute to developing a strategy to achieve healthy longevity in the future.

Can AI Detect Senescent Cells?

The study of senescent cells is not new.

According to Ms. Kono, each discovery adds tools to researchers’ ultimate fight against aging. “Science is like building a pyramid. We are just putting a block at the bottom,” Ms. Kono said. “So that’s what I’m doing, and the other scientists in this world, anywhere in this world, will read it and put another block, and the pyramid will go higher and higher, and somebody will build the drug that will contribute to longevity and health. That’s what I’m hoping for.”

In fact, researchers have for years attempted to discover the role of senescent cells and what is needed to repair cellular damage for healthy aging. Now, they are exploring new ways, including using artificial intelligence (AI).
In a study published in February in Nature Communications, researchers at the Medical Research Council Laboratory of Medical Science (LMS), in collaboration with Imperial College London and the Division of Chronic Inflammation and Cancer, German Cancer Research Center (DKFZ) in Germany, devised a family of machine-learning algorithms that take advantage of nuclear changes associated with senescence and identify senescent cells. In a news release, the authors said the advancement “promises to revolutionise treatments for cancer and aging by facilitating the development of therapies targeting senescent cells.”

Researchers said though vast strides have produced promising results in senescence research, scientists have been hampered by a lack of reliable ways to determine senescence. In their study, the researchers used nuclear morphology features of senescent cells to devise machine-learning classifiers that they claimed accurately predict senescence induced by diverse stressors in different cell types and tissues.

They reported using senescence “classifiers” to characterize drugs that either kill senescent cells, called senolytics, or to screen for drugs that selectively induce senescence in cancer cells but not normal cells.

“Virtually all cell types can be made to enter a senescent state however what senescence looks like at a cellular level, and how it can be reliably identified across thousands of cell types has been far from easy to determine,” the authors said in the news release.

But with recent advances in machine learning and AI, researchers at the LMS found they could analyze hallmarks of senescence to confirm the presence of senescent cells. They have also shown that their algorithms can be adapted to work in lab-grown cells for research and tissue samples obtained from mouse livers and patients with fatty liver disease.

Scientists worldwide have targeted senescent cells in both anti-cancer and anti-aging treatments. “Preliminary experiments in animal models have shown that the lifespans and healthspan of animals are increased when subjects are treated with so-called ‘senolytic’ drugs that attack and kill senescent cells,” researchers wrote in the news release.

In what they called “a new era of senolytic therapies,” the study authors said they could use their senescence classifiers to identify senolytics or selectively induce senescence in cancer cells in the test tube. The tool also enabled them to screen a catalog of over 600 drugs for senolytic activity, identifying several new potential therapeutic drugs.

Slowing Cell Aging

Ms. Kono said finding ways to live longer and healthier will likely happen sooner than later. “Usually, this kind of thing happens within 30 or 40 years, but aging research is quite extremely accelerated recently,” Ms. Kono said. “So many smart people are working on it. So I’m really hoping, like, in 10 years or 15 years, we might be able to develop some drug or supplemental something that will really implement extension of healthy lives in humans on Earth in this real world.”

Ms. Kono said that although human beings will still die, we have a lot to hope for while we’re living—for instance, not suffering from incurable, painful diseases until death. “We can hope for healthy longevity. This research will not extend your lifespan to 400, 500 years old. This is not the direction of our research. The direction of our research is you will be healthy until the end of your life.”

Ms. Kono likened the outcome to stories people hear about an old person just feeling “a bit sleepy” and going to lie down. A while later, their spouse comes into the room to find they have passed on, quietly and comfortably.

Ms. Kono points to the naked mole-rat as an animal that lives healthily all its life. Its social system is like that of an ant or bee, which lives in highly organized, complex societies. It can also live to be 30 years old, a lifespan roughly 10 times that of an average rat. It does not get cancer, and it maintains fertility until the end of its life.

There are many mechanisms involved in why the naked mole-rat lives so long and stays in good health, Ms. Kono said, and she intends to find out more. “One thing is they have a more robust DNA repair mechanism. Another thing, their senescent or aging cells are not accumulated in their bodies.” She speculates further that their cells may have more cushioning and sustain less damage.

The initial direction research was headed was toward killing senescent cells, Ms. Kono said, but that could cause side effects. Instead, She hopes to focus on preventing mechanical damage, thus slowing the production of senescent cells. “Then you can maintain your health longer. Ultimately, that’s the direction I’m going.”

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