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Mice blood transfusions provide new insights into senescence
A single blood transfusion from older mice into younger ones resulted in cell aging, leading to liver fibrosis, renal damage, and decreased muscle strength.
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Mice blood transfusions provide new insights into senescence
Cellular senescence is one of the responses to damage or stress when a cell enters a permanent growth arrest. Though cellular senescence serves as a protective mechanism against cancers, it notably increases with age. An increased number of senescent cells can be damaging to the organism due to their release of SASP (senescence-associated secretory phenotype), which includes inflammatory factors, growth factors, immune modulators, and protein-breaking enzymes. The SASP promotes age-related pathologies; thus, cellular senescence is recognized as one of the aging hallmarks.
The systemic effects of physiologic senescent cells in old mammals are still not clearly defined but are being extensively studied in model organisms, such as mice. One of the approaches to research them is heterochronic parabiosis – the surgical joining of young and old mice when blood, organs, and environments are shared. Previous research has shown that such joining rejuvenates older tissues while significantly aging young ones. Though several tissues were studied in such settings, the experiments mainly used artificially created senescent cells and introduced them through cell injections. So, it remained unclear to which extent naturally-occurring cellular senescence and SASP play a role in the aging transfer.
To address this question, the joint team led by Professor Jeon Ok-hee and Professor Irina Conboy comprehensively explored the effects of senescent cells induced by normal aging. The researchers aimed to establish the impact of transferring these cells from old into young animals on systemic senescence and aging.
They were able to demonstrate that the negative influence of aged circulation outweighed the benefits of young circulation, particularly in brain and liver tissues. The study showed that multiple SASP factors trigger the aging of cells, leading to liver fibrosis, renal damage, and decreased muscle strength. Notably, the effect was significant in young animals even after a single exchange. The researchers also demonstrated that treatment with senolytic drugs before blood exchange could revoke the induction of senescence. If old animals were treated before the exchange, it attenuated the pro-geronic influence on young mice.
This study shifts theparadigm toward regarding cellular senescence more as a systemic process. From this point of view, senescence is not only age-dependent but also can spread, affecting multiple tissues. Such systemic induction of senescence can significantly accelerate aging. These findings might provide insights for designing new senolytic drugs specifically targeted at senescent factors in the blood.
Source Nature Metabolism
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Mice blood transfusions provide new insights into senescence
Cellular senescence is one of the responses to damage or stress when a cell enters a permanent growth arrest. Though cellular senescence serves as a protective mechanism against cancers, it notably increases with age. An increased number of senescent cells can be damaging to the organism due to their release of SASP (senescence-associated secretory phenotype), which includes inflammatory factors, growth factors, immune modulators, and protein-breaking enzymes. The SASP promotes age-related pathologies; thus, cellular senescence is recognized as one of the aging hallmarks.
The systemic effects of physiologic senescent cells in old mammals are still not clearly defined but are being extensively studied in model organisms, such as mice. One of the approaches to research them is heterochronic parabiosis – the surgical joining of young and old mice when blood, organs, and environments are shared. Previous research has shown that such joining rejuvenates older tissues while significantly aging young ones. Though several tissues were studied in such settings, the experiments mainly used artificially created senescent cells and introduced them through cell injections. So, it remained unclear to which extent naturally-occurring cellular senescence and SASP play a role in the aging transfer.
To address this question, the joint team led by Professor Jeon Ok-hee and Professor Irina Conboy comprehensively explored the effects of senescent cells induced by normal aging. The researchers aimed to establish the impact of transferring these cells from old into young animals on systemic senescence and aging.
They were able to demonstrate that the negative influence of aged circulation outweighed the benefits of young circulation, particularly in brain and liver tissues. The study showed that multiple SASP factors trigger the aging of cells, leading to liver fibrosis, renal damage, and decreased muscle strength. Notably, the effect was significant in young animals even after a single exchange. The researchers also demonstrated that treatment with senolytic drugs before blood exchange could revoke the induction of senescence. If old animals were treated before the exchange, it attenuated the pro-geronic influence on young mice.
This study shifts theparadigm toward regarding cellular senescence more as a systemic process. From this point of view, senescence is not only age-dependent but also can spread, affecting multiple tissues. Such systemic induction of senescence can significantly accelerate aging. These findings might provide insights for designing new senolytic drugs specifically targeted at senescent factors in the blood.
Source Nature Metabolism
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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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