RE: News aus der Forschung - 5

Zitat von Prometheus im Beitrag #96

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Zitat von Speedy im Beitrag #95

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Vagus nerve control of HMGB1 accessibility: a bioelectronic strategy for inflammation and pain
https://link.springer.com/article/10.1186/s42234-026-00209-9

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Zitat

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Die Vagusnervstimulation stellt eine Intervention dar, die den Eintritt von Entzündungszellen einschränken und die nachgeschaltete Signalübertragung dämpfen kann. Vor allem aber liefert sie eine klare und überprüfbare klinische Hypothese: Wenn die Zugänglichkeit von HMGB1 ein regulierter Schlüssel für Entzündung und Schmerz ist, könnten klinische Studien zur Vagusnervstimulation neben Zytokinen auch andere Biomarker nutzen, indem sie Veränderungen der HMGB1-Mobilisierung, der Komplexbildung und klinisch relevante Schmerzparameter einbeziehen.

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@Speedy , @alle

Nutzt jemand Vagusnervstimulation?

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Vor einem Jahr etwa gebraucht den Sensate 2 gekauft. Kaum eingesetzt allerdings bislang. Sollte ich vielleicht mal ändern. Hatte eher rein auf Eiswürfel gesetzt.

Therapeutic inhibition of telomeric DNA damage response rescues hematopoietic dysfunction driven by telomere shortening and aging
https://www.nature.com/articles/s43587-0..._a1demo0jtae9sy

Noninvasive Neuromodulation and Neuroimaging to Enhance Glymphatic Function for Neurodegenerative and Autoimmune Disorders in Next-Generation Personalized Treatments and Precision Neuropsychiatry: A Perspective Proposal
https://www.mdpi.com/2076-3417/16/13/6593

The cGAS-STING pathway: Mechanism and medical implications
https://www.cell.com/cell/fulltext/S0092...NCg2jZEGnt8ghGQ

Mechanisms and interventions of epigenetic aging
https://www.cell.com/cell-chemical-biolo...2mls8JJDnK2nEdw

The cancer Alzheimer’s disease paradox
https://www.nature.com/articles/s41514-0...tVpt2vUw0av-ENA

Hallo Speedy,

wenn die genauen Ursachen bekannt sind, ist das sog. Paradoxon evtl. nicht mehr so ungewöhnlich.

VG

Roger

Declines in mRNA synthesis set the rate of organismal aging
https://www.biorxiv.org/content/10.64898...4RPhBV-ksAHAqQw

Hypoxia rescues complex 1-associated disease caused by proteostatic defects
https://www.nature.com/articles/s42255-0...eeS0pla-O5UYyQw

Proteostasis Rebalancing by LET-607 Deficiency Promotes Longevity
https://onlinelibrary.wiley.com/doi/full...ABZGgqEwddy5PqA

Zitat

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Melanin is ubiquitous across kingdoms and has light-absorbing and redox properties.
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Melanin's light-absorbing and signaling properties regulate neuroendocrine communication.
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Melanin links light, microbes and neuroendocrinology via the melanocortin pathway.
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Gut microbes modulate the melanocortin pathway via gut-brain-skin signaling.
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A circadian disrupted-melanocortin pathway disrupts the gut–brain-skin axis.

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Light, melanin, and the microbial clock: Rewiring the gut–brain–skin axis
https://www.sciencedirect.com/science/ar...091302226000415

Zitat von Speedy im Beitrag #108

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Proteostasis Rebalancing by LET-607 Deficiency Promotes Longevity
https://onlinelibrary.wiley.com/doi/full...ABZGgqEwddy5PqA

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Zitat

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Our findings establish the platelet-CD47-monocyte axis as a pivotal pathway for healthy aging and reveal recombinant LAV-BPIFB4 as a promising therapeutic approach for managing inflammaging and cardiovascular disease by harnessing the immune-tuning capacity characteristic of exceptional longevity.

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The LAV-BPIFB4-Platelet-CD47 Axis: A Novel Mechanism Associated With Immune Resilience in Longevity
https://onlinelibrary.wiley.com/doi/10.1...TmG2UUKKaa_Q_sw

Lawnmower-like Enzyme Rewinds Decades of Molecular Aging in Human Tissue
https://www.the-scientist.com/lawnmower-...an-tissue-74728

Combating ageing beyond the cell: Emerging roles of extracellular proteostasis
https://febs.onlinelibrary.wiley.com/doi...1N20vRg3vJjU_0Q

Zitat

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Muscle-derived Mimecan regulates core body temperature via brown adipose tissue
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Mimecan activates MC4R-positive neurons in the DMH/DHA via maintaining primary cilia
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Restoring plasma Mimecan levels counteracts aging and promotes lifespan in aged mice
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Voluntary exercise improves core body temperature regulation via maintaining Mimecan

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Muscle-derived Mimecan regulates hypothalamus-brown adipose tissue communication and promotes health and lifespan in mice
https://www.cell.com/cell-metabolism/ful...7XAtKR-L8SA_s0A

Zitat

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This work identifies EP2 signaling in TRMs as a central regulator of organ-wide aging through its control of senescent neutrophil clearance, reframing aging as a failure of active cellular clearance rather than passive degeneration.

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Restored clearance of senescent neutrophils by tissue-resident macrophages limits organ aging
https://www.science.org/doi/10.1126/scie...nwWsQaRCN0iK4wg

EP2 wurde in dieser Studie mit einer experimentellen Substanz gehemmt. Leider ist mir keine verfügbare Substanz bekannt mit der ebenfalls eine direkte Hemmung möglich wäre.

Multiomic profiling of responses to clinical and novel bisphosphonates reveals extraskeletal effects on ageing related signatures
https://www.nature.com/articles/s41392-0..._a1demo0jtae9sy

Zitat von Speedy im Beitrag #117

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Multiomic profiling of responses to clinical and novel bisphosphonates reveals extraskeletal effects on ageing related signatures
https://www.nature.com/articles/s41392-0..._a1demo0jtae9sy

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Scientists find compound that may help muscles stay strong as we age
https://medicalxpress.com/news/2026-07-s...j8AIb5QSciXoJ_Q

Chromosome-protecting protein may help explain muscle repair and the rarity of muscle cancers
https://medicalxpress.com/news/2026-07-c...6Tgm7cnuhSXJ7pA

TRF2 ist hier gemeint.

Zitat

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Exercise-induced ROS act as essential signaling molecules that mediate the widespread metabolic and physiological benefits of exercise.
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In skeletal muscle, exercise-induced ROS activates adaptive pathways, including AMPK, PGC-1α, and NRF2.
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Excessive antioxidant buffering may impair responsiveness to physiological ROS signaling, promoting redox resistance.
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Pancreatic β-cells illustrate the importance of physiological ROS signaling in insulin secretion and metabolic homeostasis.

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From ROS Signaling to Redox Resistance in Exercise and Metabolic Disease
https://www.sciencedirect.com/science/ar...666337626000983

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Endothelial dysfunction was induced combining Ang-II and shear flow stress.
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Green photobiomodulation treatments improved endothelial survival.
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Green photobiomodulaton treatments elevated ROS levels and recovered NO expression.
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PBM treatments can rescue acute endothelial dysfunction.

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A Novel Acute Microphysiological model of Endothelial Dysfunction rescued by Green Laser Photobiomodulation Treatment
https://www.sciencedirect.com/science/ar...666469026000333

Zitat

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Collectively, these findings demonstrate that ASAP3 is a novel regulator of liver aging, promoting senescence and impairing autophagy and mitochondrial function by disrupting actin cytoskeleton dynamics.

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ASAP3 deficiency alleviates hepatic senescence and correlates with extended healthspan in mice
https://pubmed.ncbi.nlm.nih.gov/42431471/

Zitat

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Telomere shortening induces brain aging hallmarks and cognitive impairment
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sDLK1 is identified from senescent microglia with shortened telomeres in vitro and in mice
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CSF sDLK1 is elevated in aged mice, and its overexpression drives hypomyelination
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sDLK1 impairs oligodendrocyte maturation and neuronal activity in a human iPSC model

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Senescent microglia with shortened telomeres secrete soluble DLK1 to induce aging-associated hypomyelination and neuronal dysfunction
https://www.cell.com/neuron/fulltext/S08...-JgCG2xIdx8LvRA

Overexpression of xanthine dehydrogenase extends lifespan in C. elegans
https://www.micropublication.org/journal...P6ccb7Nu3KnNYrg