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The connection between the cystine/glutamate antiporter system and life extension in mice
Targeting the cystine/glutamate antiporter system xc- is a promising strategy to promote healthy aging.
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The cystine/glutamate antiporter system xc− is responsible for exchanging intracellular glutamate for extracellular cystine, modulation of glutamatergic neurotransmission in mice's central nervous system (CNS), and neuroinflammation. Genetic deletion of the specific subunit of the system called xCT (xCT-/-) in mouse models is protective for age-related neurological disorders characterized by excitotoxicity and neuroinflammation. Researchers observed visible oxidative shift in adult mice's plasma cystine/cysteine ratio with genetic deletion of xCT (xCT-/- mice), which led to the hypothesis that system xc- deletion would negatively impact mice lifespan and healthspan. The role of system xc- in physiological aging is still mostly unknown.
Lise Verbruggen et al. researched the impact of xCT deletion on the aging process of mice, with a particular focus on hippocampal function, the immune system, and cognitive aging. The team observed that male xCT-/- mice have an extended lifespan, despite an even more increased plasma cystine/cysteine ratio in aged mice compared to adult mice.
The observed oxidative shift did not negatively impact the general health status of the mice. On the contrary, the innate immune system's age-related priming (immune system memory building) usually manifested as increased cytokine levels and hypothermia in xCT+/+ mice treated with lipopolysaccharide (LPS), was attenuated in xCT-/- mice. The absence of system xc – also altered the hippocampal metabolome, with only minor effects on hippocampal inflammation in aged mice.
The article was first-time proof that male mice that age in the absence of system xc− have an extended lifespan and decreased priming of the peripheral immune system. They are also protected against age-related decline in hippocampal function and memory, a known feature of aging with a disastrous impact on the elderly. Verbruggen et al. suggest that reduced priming of the immune system in aged xCT−/− mice and the improved metabolic state of the aged xCT−/− hippocampus could be beneficial for other age-related impairments. Therefore, targeting system xc- is a promising strategy to prevent cognitive decline and to promote healthy aging.
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The cystine/glutamate antiporter system xc− is responsible for exchanging intracellular glutamate for extracellular cystine, modulation of glutamatergic neurotransmission in mice's central nervous system (CNS), and neuroinflammation. Genetic deletion of the specific subunit of the system called xCT (xCT-/-) in mouse models is protective for age-related neurological disorders characterized by excitotoxicity and neuroinflammation. Researchers observed visible oxidative shift in adult mice's plasma cystine/cysteine ratio with genetic deletion of xCT (xCT-/- mice), which led to the hypothesis that system xc- deletion would negatively impact mice lifespan and healthspan. The role of system xc- in physiological aging is still mostly unknown.
Lise Verbruggen et al. researched the impact of xCT deletion on the aging process of mice, with a particular focus on hippocampal function, the immune system, and cognitive aging. The team observed that male xCT-/- mice have an extended lifespan, despite an even more increased plasma cystine/cysteine ratio in aged mice compared to adult mice.
The observed oxidative shift did not negatively impact the general health status of the mice. On the contrary, the innate immune system's age-related priming (immune system memory building) usually manifested as increased cytokine levels and hypothermia in xCT+/+ mice treated with lipopolysaccharide (LPS), was attenuated in xCT-/- mice. The absence of system xc – also altered the hippocampal metabolome, with only minor effects on hippocampal inflammation in aged mice.
The article was first-time proof that male mice that age in the absence of system xc− have an extended lifespan and decreased priming of the peripheral immune system. They are also protected against age-related decline in hippocampal function and memory, a known feature of aging with a disastrous impact on the elderly. Verbruggen et al. suggest that reduced priming of the immune system in aged xCT−/− mice and the improved metabolic state of the aged xCT−/− hippocampus could be beneficial for other age-related impairments. Therefore, targeting system xc- is a promising strategy to prevent cognitive decline and to promote healthy aging.
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Dr. Ana Baroni MD. Ph.D.
Scientific & Medical Advisor
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Ana has over 20 years of consultancy experience in longevity, regenerative and precision medicine. She has a multifaceted understanding of genomics, molecular biology, clinical biochemistry, nutrition, aging markers, hormones and physical training. This background allows her to bridge the gap between longevity basic sciences and evidence-based real interventions, putting them into the clinic, to enhance the healthy aging of people. She is co-founder of Origen.life, and Longevityzone. Board member at Breath of Health, BioOx and American Board of Clinical Nutrition. She is Director of International Medical Education of the American College of Integrative Medicine, Professor in IL3 Master of Longevity at Barcelona University and Professor of Nutrigenomics in Nutrition Grade in UNIR University.
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