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How ageing promotes metastasis

The study shows how aging alters the biology of lung cancer and makes tumors more prone to spreading. The researchers identified a molecular signaling pathway, a complex chain of reactions and interactions, in which a specific stress-response protein, ATF4, plays a central role.

Under normal physiological conditions, ATF4 acts as a hub for the “integrated stress response” that responds to events such as nutrient deprivation, viral particles, or the accumulation of misfolded proteins, activating protective and corrective responses, explains the author.

“In older patients, this stress response is hijacked by the tumor, allowing cancer cells to reprogram their metabolism. The tumor does not grow faster, but this metabolic rewiring enables the cancer cells to spread and form metastases in other parts of the body,” the author says.

Tumors from older individuals in the study, both mice and humans, showed higher levels of ATF4. High ATF4 levels were also associated with increased recurrence after lung surgery and poorer survival among patients with lung adenocarcinoma, the most common form of lung cancer.

“Our results suggest that ATF4 is not only part of the mechanism behind the spread of lung cancer but may also serve as a marker of more aggressive disease,” says another author.

The study opens the door to a treatment strategy targeting the age-related signaling system that the tumor has hijacked. By blocking ATF4, or a specific metabolic process controlled by ATF4, with drugs, the researchers were able to dramatically reduce the spread of old tumors in mice.

Previously, it has been unclear why studies using similar drugs have largely failed when tested in humans. The new findings suggest that these treatments may need to be targeted more precisely to the right patient groups. ScienceMission sciencenewshighlights.

Vitamin C inhibits ACSL4 to alleviate ferro-aging in primates

Liu et al. identify that an iron-triggered aging pathway, termed ferro-aging, is orchestrated by ACSL4. Vitamin C directly targets and inhibits ACSL4, thereby blocking ferro-aging. Their further research shows that long-term supplementation in non-human primates systemically attenuates aging and improves metabolic and neurological function.

Clearing circular RNA from cells extends lifespan, C. elegans study reveals

Cells in our bodies produce RNA based on genetic information stored in DNA, and RNA serves as a blueprint for making proteins. Researchers at KAIST have discovered a new phenomenon: Removing “circular RNA” that accumulates in cells as we age can slow down aging and extend lifespan. This study provides crucial clues for uncovering the principles of aging and developing treatment strategies for related diseases.

Professor Seung-Jae V. Lee’s research team (RNA-Mediated Healthspan and Longevity Research Center) from the Department of Biological Sciences, in collaboration with research teams led by Professors Yoon Ki Kim and Gwangrog Lee, discovered the RNASEK protein —an enzyme that degrades circular RNA—plays a vital role in slowing aging and extending lifespan. The findings are published in the journal Molecular Cell.

Until now, circular RNA was primarily known as a “marker of aging” because of its high stability, causing it to accumulate in cells without being degraded as one ages. However, the molecular mechanism for removing this RNA and its direct link to aging had not been clearly identified. The research team conducted this study to determine how the accumulation of circular RNA affects aging and whether an intracellular management system exists to regulate it.

Study suggests one common amino acid may affect how long men live

A large new study suggests that higher levels of a common amino acid called tyrosine may be linked to a shorter lifespan in men.

The research, published recently in the journal Aging, examined whether blood levels of two amino acids, phenylalanine and tyrosine, were connected to how long people live.

Amino acids are building blocks of protein. They are found in protein-rich foods such as milk, eggs and meat, and are also sold as dietary supplements.

How Zinc Protects Injured Arteries From Accelerated Aging

Researchers publishing in Aging Cell have discovered that the nuclei of the cells that line injured arteries quickly become misshapen and that this leads to accelerated cellular senescence. Delivering zinc to these cells partially alleviates this dysmorphism.

Two seemingly unrelated concepts

This paper begins with a discussion of two different concepts that, on the surface, appear to be unrelated. First, the researchers discuss vascular damage, particularly in the context of surgeries; even minimally invasive procedures that involve cutting, scraping, or burning arteries must cause some level of damage. This includes such procedures as catheter implantation as a treatment for heart disease [1] and the resection of cancerous tumors [2].

Exercise Triggers Memory-Related ‘Brain Ripples’, Study Finds

Exercise works wonders throughout the human body, including the brain.

Research suggests an array of neurological benefits, such as reducing the brain’s biological age, enhancing learning and memory, and protecting against dementia.

Now, a new study offers one of the clearest glimpses yet into a suspected mechanism: after a single 20-minute session of light-to-moderate cycling, people showed changes in memory-linked brain activity.

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