RE: News aus der Forschung - 6

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STING pathway is not activated in telomerase-deficient mice with short telomeres
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p53 activation in telomerase-deficient mice with short telomeres is STING independent
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STING does not mediate aging phenotypes associated with short telomeres in mice

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STING deficiency does not rescue short telomere-mediated aging phenotypes and longevity in TERC- or TERT-telomerase deficient mice
https://www.cell.com/cell-reports/fullte...pEQemiftzamIjlw

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Our results identify TIMP2 as a modulator of age-associated microglia dysfunction. Harnessing its activity may mitigate detrimental effects of age-associated insults on microglia function.

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Youth-associated protein TIMP2 regulates microglial state and function in healthy and aged mice
https://www.nature.com/articles/s41467-0..._a1demo0jtae9sy

Gemfibrozil promotes longevity and health by restricting amino acid uptake through the Dipeptide transporter, PEPT1
https://www.nature.com/articles/s41514-026-00474-7

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Collectively, our findings identify ANGPTL8 as an endocrine regulator linking metabolic dysfunction to adipose tissue senescence and systemic aging, highlighting the ANGPTL8-AKT2-mTOR axis as a potential therapeutic target for delaying age-associated functional decline.

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An ANGPTL8-AKT2-mTOR Axis Drives Adipose Senescence and Aging-Related Functional Decline
https://pmc.ncbi.nlm.nih.gov/articles/PMC13478719/

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Our findings establish the LMNA-CK2-STING axis as a key biochemical mechanism that suppresses innate immune activation at the NE, offering a promising strategy for ameliorating aging and progeroid pathologies.

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CK2α restriction of STING accumulation underlies systemic aging
https://www.nature.com/articles/s41467-026-76351-4

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These findings demonstrate a role for CCND1/CDK6 in regulating DNA damage and inflammation in senescence and aging, highlighting it as a promising target for therapeutic repurposing.

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Inhibiting cyclin D1–CDK6 suppresses senescence-associated inflammatory gene expression and age-related functional decline
https://www.nature.com/articles/s43587-0..._a1demo0jtae9sy

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Our study provides preclinical evidence supporting dioscin as a novel intervention that ameliorates aging-associated phenotypes and highlights the pivotal role of UPRER in lifespan extension and aging suppression.

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Dioscin extends lifespan and ameliorates aging associated phenotypes in association with the endoplasmic reticulum unfolded protein response
https://pubmed.ncbi.nlm.nih.gov/42575256/

Mit Yamswurzel oder Bockshornklee (@Tizian) ist man gut dabei.

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Late-life semaglutide treatment slows ageing and extends lifespan in female mice
https://www.nature.com/articles/s41586-0...LPgRqEt5ZZ0c-EQ

Assessing mechanisms and evidence of a causal role for cellular senescence and somatic mutations in aging
https://www.aging-us.com/article/206414/...FpCwzIxIcUGLfNg

Physical Exercise in Immunotherapy
https://link.springer.com/article/10.1186/s40798-026-01101-1

Nature Biotechnology | Insilico’s AI-Driven IPF Candidate Rentosertib Shows Potential for Biological Age Reversal, as Assessed by Six Proteomic Aging Clocks
https://insilico.com/news/rnt0709261-ren...ic-aging-clocks

TNIK-Hemmung hatten wir ja schon des Öfteren hier im Forum besprochen.

Zitat

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Physiological aging results in widespread changes in RNA processing, degradation, modifications, and translation in the nervous system.

Corresponding changes in RNA-binding protein regulatory networks and aberrant ribonucleoprotein granule dynamics contribute to RNA dysregulation.

Age-related RNA dysregulation may predispose neurons to declining function and neurodegeneration.

Understanding how aging reshapes RNA regulatory networks will reveal new therapeutic opportunities for neurodegenerative disease

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RNA dysregulation as a determinant of aging and neurodegenerative vulnerability
https://www.cell.com/trends/cell-biology...R_5ki_WF2cSCyrw

Core regulatory pathways of natural products in anti-aging: Research progress at molecular, cellular, and systemic levels
https://www.sciencedirect.com/science/ar...095177926002509