RE: Senolysis, Reloaded - 7

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These findings establish macrophage senescence as a central driver of chronic inflammation in aging and metabolic liver disease, and a tractable therapeutic target.

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p21+TREM2+ senescent macrophages fuel inflammaging and metabolic dysfunction-associated steatotic liver disease
https://www.nature.com/articles/s43587-0...8_v0_s00_e0_tv0

Cellular senescence: from pathogenic mechanisms to precision anti-aging interventions
https://www.aging-us.com/article/206375/text

Targeting Age-Associated Immune Senescence via Nanoparticle-Based Metabolic Reprogramming
https://pubs.acs.org/doi/10.1021/acsnano...Og6SyRtGkoi93Gg

Eine Zusammenfassung zu Tomatidin noch mal.

Green Gold: Tomatidine Reverses Cognitive Decline by Mending the Leaky Brain
https://www.rapamycin.news/t/green-gold-...aky-brain/24776

Salvianolic acids are natural senolytics and increase lifespan in old age
https://www.biorxiv.org/content/10.64898/2026.04.29.721790v1

Zitat

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Distinct senescent states arise across brain-barrier cell lineages
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Endothelial cells and macrophages engage a transient inflammatory senescent state
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Choroid plexus epithelium maintains a persistent non-inflammatory senescent state
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Senescent cell ablation alters vascular patterning and CSF homeostasis

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Persistent and transient senescent cells contribute to brain-barrier development
https://www.cell.com/cell/fulltext/S0092...v-kaqQoQ1Xa8xkQ

Synergistic senolytic–regenerative therapy significantly extends healthspan and lifespan
https://link.springer.com/article/10.118...CosrqV9ENPb6tdw

Was genau ist das SenoVax™ eigendlich? Es wird gespritzt? In die Vene? In den Muskel? Und was sind da für Dinge drin?

Zitat

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These results suggest that activation of p38MAPK plays a role in regulating skeletal muscle senescence and that DNA damage-induced senescence in iPSC-derived myocytes represents a viable model for studying human skeletal muscle senescence.

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p38MAP kinase regulates senescence in human iPS-derived myocytes
https://www.aging-us.com/article/206385/text

Multi-omics profiling reveals systemic rejuvenation of the aged kidney through senolytic therapy
https://www.nature.com/articles/s41536-0..._a1demo0jtae9sy

Nanoparticles as an efficient strategy to eliminate senescent brain endothelial cells
https://www.sciencedirect.com/science/ar...168365926005778

Could this enzyme help remove 'zombie' cells from our tissues?
https://medicalxpress.com/news/2026-07-e...Qs0eh0F4sGaACsQ

Zitat

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Together, these findings identify a mitochondrial metabolic checkpoint that enables the epigenetic execution of innate immune signalling, revealing a mechanism that selectively controls the inflammatory output of senescent cells.

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Mitochondrial metabolism and epigenetic crosstalk drive SASP
https://www.nature.com/articles/s41586-0...dgQcHlUW7jHzOqg

Parthenolid (Mutterkraut) hemmt als natürliche Substanz SLC25A1.

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Senomorphic agents modulate SASP without eliminating senescent cells.
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A hierarchical sensor–hub–effector model of SASP regulation is proposed.
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Translational barriers of senomorphic agents are critically analyzed.
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A “clearance-first, modulation-later” synergistic strategy is introduced.
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Therapeutic potential in neurodegenerative, skeletal, and metabolic ageing is discussed.

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Senomorphic agents: Multi-target strategies to tame the senescence-associated secretory phenotype for healthy ageing
https://www.sciencedirect.com/science/ar...Afg&via%3Dihub=

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Nutritional interventions predominantly modulate SASP in humans.
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Calorie restriction showed the most consistent anti-senescence effects.
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Telomere length showed limited responsiveness across interventions.
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n-3 polyunsaturated fatty acids reduced multiple SASP components.
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Multi-marker frameworks are needed for senescence assessment in humans.

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Effects of nutritional interventions on biomarkers of cellular senescence in humans: A systematic review
https://www.sciencedirect.com/science/ar...568163726002163

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PD-L2 is an immune checkpoint upregulated by senescent cells with aging
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Circulating soluble PD-L2 increases with aging and declines after senolytics in humans
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Mice lacking PD-L2 accumulate fewer senescent cells during aging
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Blocking PD-L2 function increases insulin sensitivity and physical strength

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Blocking PD-L2 prevents senescent cell accumulation and age-related dysfunction
https://www.cell.com/cell-metabolism/abs...KAO0Hy8K6qSPVOw

Zitat

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Overall, our study provides the core gene-regulatory principles underlying a senescent-like transitional state in monocytes and identifies AP-1 as an attractive target to modulate systemic inflammation in age and disease.

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A transitional senescence program drives inflammatory monocyte state expansion in aging humans
https://www.biorxiv.org/content/10.64898...VbFHLP8LqqwoNiw

#171
Mit Curcumin ist man fast überall gut dabei.

Hier noch weitere natürliche AP-1 - Hemmer wie Withaferin A, Celastrol oder Quercetin:
https://www.scbt.com/browse/ap1-inhibito...SXSqyzJSUgxZ1ev