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Category: life extension

Unlocking the skin’s natural healing power for regenerative medicine

Our skin protects us from everyday mechanical stresses, like friction, cuts, and impacts. A key part of this function—standing as a bulwark against the outside world—is the skin’s amazing ability to regenerate and heal. But where does this healing ability begin?

In a new study published in Nature Communications, an interdisciplinary team led by the laboratories of Kaelyn Sumigray, Ph.D., and Stefania Nicoli, Ph.D., discovered that, during the earliest stages of embryonic development, contribute to forming a protective skin layer that accelerates healing as the embryo grows.

Their findings reveal one of the earliest steps in how skin stem cells learn to repair tissue—knowledge that could help engineer improved for transplantation.

Therapeutic strategies targeting cellular senescence for cancer and other diseases

Cellular senescence occurs in response to endogenous or exogenous stresses and is characterized by stable cell cycle arrest, alterations in nuclear morphology and secretion of proinflammatory factors, referred to as the senescence-associated secretory phenotype (SASP). An increase of senescent cells is associated with the development of several types of cancer and aging-related diseases. Therefore, senolytic agents that selectively remove senescent cells may offer opportunities for developing new therapeutic strategies against such cancers and aging-related diseases. This review outlines senescence inducers and the general characteristics of senescent cells. We also discuss the involvement of senescent cells in certain cancers and diseases. Finally, we describe a series of senolytic agents and their utilization in therapeutic strategies.

What’s The Biochemistry Of Fitness In 80yr Olds?

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DNA repair mechanisms help explain why naked mole-rats live a long life

Naked mole-rats are one of nature’s most extraordinary creatures. These burrowing rodents can live for up to 37 years, around ten times longer than relatives of a similar size. But what is the secret to their extreme longevity? How are they able to delay the decay and decline that befalls other rodents? The answer, at least in part, is due to a switch in a common protein that boosts DNA repair, according to new research published in the journal Science.

One of the main causes of aging in all animals, including humans, is the accumulation of damaged DNA, our genetic instruction manual. When this damage is not fixed, it leads to , damaged proteins and eventually a breakdown in the body’s functions.

To understand how the naked mole-rat is so resistant to DNA damage, a study led by researchers at Tongji University in China focused on a common protein called cGAS (cyclic GMP-AMP synthase). In most mammals, cGAS interferes with DNA repair, but the researchers suspected it may have evolved a different function in the long-living rats.

Holocene skeletal samples challenge link between sedentary lifestyles and age-related bone weakening

Research led by Vladimír Sládek sheds new light on how bones age, questioning long-standing assumptions that sedentary lifestyles are the primary cause of weakening bone strength in modern humans.

The study analyzed 1,881 adult humeri, femora, and tibiae from European Holocene populations to examine how and structure change with age. Surprisingly, researchers found that patterns of diaphyseal (shaft) aging were consistent across both Early and Late Holocene adults—despite significant differences in physical activity levels between the two groups. The research is published in the journal Science Advances.

“Our findings suggest that lifestyle differences may not fully explain age-related declines in bone strength,” said Dr. Sládek. “Instead, the biology of bone growth and aging itself plays a critical role.”

A cGAS-mediated mechanism in naked mole-rats potentiates DNA repair and delays aging

Efficient DNA repair might make possible the longevity of naked mole-rats. However, whether they have distinctive mechanisms to optimize functions of DNA repair suppressors is unclear. We find that naked mole-rat cyclic guanosine monophosphate–adenosine monophosphate synthase (cGAS) lacks the suppressive function of human or mouse homologs in homologous recombination repair through the alteration of four amino acids during evolution. The changes enable cGAS to retain chromatin longer upon DNA damage by weakening TRIM41-mediated ubiquitination and interaction with the segregase P97. Prolonged chromatin binding of cGAS enhanced the interaction between repair factors FANCI and RAD50 to facilitate RAD50 recruitment to damage sites, thereby potentiating homologous recombination repair.

Age-Defying Health Benefits: New Research Unravels Secrets of the “Longevity” Gene

Deleting the S6K1 protein in mice reduces inflammation and extends lifespan by suppressing inflammatory proteins, highlighting a new mechanism in aging and potential treatments for age-related diseases. S6K1 is a protein that plays a role in regulating aging and age-related diseases. Inhibiting t

Mitochondrial building block balance linked to age-related inflammation

Research led by the Max Planck Institute for Biology of Aging in Cologne reports that misincorporation of ribonucleotides into mitochondrial DNA (mtDNA) initiates an inflammatory cascade.

Mitochondria support cell survival through metabolic and signaling roles. Conversely, their disruption has been associated with inflammation, and disease.

Innate immune activation through the cGAS-STING-TBK1 pathway can move a cell from short-term defense to a chronic state of alarm. cGAS-STING activity is linked to autoimmune and inflammatory diseases and contributes to senescence and aging, intertwining immune signaling with tissue decline.

A New Class of Drug Created That Fights Aging on a Cellular Level

Scientists continue to explore ways we can live longer and ensure those lives are healthier. A new discovery of note in this field comes from experiments in fission yeast (an organism often used for studies of aging).

Researchers from Queen Mary University of London have been testing a new drug called Rapalink-1, building on an existing immunosuppressant called rapamycin that has been shown to extend the life of cells and rodents. In these new tests, Rapalink-1 extended yeast lifespan to a similar degree as rapamycin.

What’s more, molecular analysis revealed that the drug increased the production of enzymes that convert a compound made by gut bacteria, called agmatine, into a variety of other chemicals.

Pan-disease atlas maps molecular fingerprints of health, disease and aging

A new study has mapped the distinct molecular “fingerprints” that 59 diseases leave in an individual’s blood protein, which could enable blood tests to discern troubling signs from those that are more common.

As now published in Science, an international team of researchers mapped how thousands of proteins in human blood shift as a result of aging and serious diseases, such as cancer and cardiovascular and .

The Human Disease Blood Atlas also reveals that each individual’s blood profile has a unique molecular fingerprint, which changes through childhood and stabilizes in adulthood. This provides a baseline for comparison that could one day use to flag early deviations.

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