Verschiedenes » Knochenmark

Dem Knochenmark haben wir bisher noch wenig Aufmerksamkeit geschenkt, obwohl es bzw. seine Reduktion ein wesentlicher Faktor der Alterung sein dürfte, denn dort sitzen viele Stammzellen.

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The depletion of bone marrow cellularity begins at birth and continues to decline with age. At 50 years of age the average cellularity is 50 %; however, wide ranges of 30–70 % have been observed [69]. This highlights the importance of the bone marrow milieu in the aging hematopoietic system.

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https://www.cell.com/heliyon/fulltext/S2405-8440(24)08862-5

Restoring bone marrow niche function rejuvenates aged hematopoietic stem cells by reactivating the DNA Damage Response

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We identify Netrin-1 as a critical regulator of BM niche cell aging. Niche-specific deletion of Netrin-1 induces premature aging phenotypes within the BM microenvironment, while supplementation of aged mice with Netrin-1 rejuvenates aged niche cells and restores competitive fitness of aged blood stem cells to youthful levels. We show that Netrin-1 plays an essential role in maintaining active DNA damage responses (DDR), and that aging-associated decline in niche-derived Netrin-1 results in DNA damage accumulation within the BM microenvironment. We show that Netrin-1 supplementation is sufficient to resolve DNA damage and restore regenerative potential of the aged BM niche and blood stem cells to endure serial chemotherapy regimens.

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https://www.nature.com/articles/s41467-023-37783-4

Aged bone marrow macrophages drive systemic aging and age-related dysfunction via extracellular vesicle-mediated induction of paracrine senescence

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Here we found that physiologically aged bone marrow monocytes/macrophages (BMMs) propagate senescence to multiple tissues, through extracellular vesicles (EVs), and drive age-associated dysfunction in mice. We identified peroxisome proliferator-activated receptor α (PPARα) as a target of microRNAs within aged BMM-EVs that regulates downstream effects on senescence and age-related dysfunction. Demonstrating therapeutic potential, we report that treatment with the PPARα agonist fenofibrate effectively restores tissue homeostasis in aged mice. Suggesting conservation to humans, in a cohort study of 7,986 participants, we found that fenofibrate use is associated with a reduced risk of age-related chronic disease and higher life expectancy.

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https://www.nature.com/articles/s43587-024-00694-0

https://www.sciencedirect.com/science/ar...1125?via%3Dihub
Die Wasserstoffgasbehandlung verlängert die replikative Lebensdauer multipotenter Stromazellen des Knochenmarks in vitro und bewahrt gleichzeitig die Differenzierung und parakrine Potenziale
Mein running Gag...aber es steht auch...
Interessanterweise verringerte eine 3 %ige Wasserstoffgasbehandlung Hydroxylradikale, Proteincarbonyl und 8-Hydroxydesoxyguanosin nicht, was darauf hindeutet, dass das Abfangen von Hydroxylradikalen in dieser Studie möglicherweise nicht für diese Wirkungen von Wasserstoffgas verantwortlich ist.
Also vielleicht doch mehr als stumpfes Vitamin C.
Und halt in Vitro, yummy Knochensuppe.