Advanced glycation end products

1. Advanced glycation end products induce cellular senescence in human cells.

   “Concurrent treatment with high glucose and AGEs substantially suppressed SHED proliferative and migratory capacity while simultaneously enhancing apoptotic cell death and cellular senescence.”

   Cellsunder high-glucose conditions

   AGEs derived from high-sugar diets induce functional impairment of odontogenic stem cells via RAGE-mediated endoplasmic reticulum stress

   Histochemistry and cell biology·24 May 2026

2. Advanced glycation end products increase cellular senescence in cells.

   “In a co-culture system, AGE-treated osteoclasts accelerated chondrocyte senescence, as evidenced by elevated senescence markers and SASP factors.”

   Cellsin co-culture

   SIRT1 Downregulation by Advanced Glycation End Products Activates RANKL-Dependent Osteoclast Signaling and Drives Chondrocyte Senescence During Osteoarthritis Development

   Aging cell·1 May 2026

3. Advanced glycation end products increase cellular senescence in human cells.

   “AGEs treatment significantly exacerbated hGC senescence, impaired mitochondrial function, and suppressed mitophagy in a concentration-dependent manner.”

   Cellsconcentration-dependent

   SIRT3 attenuates AGEs-induced senescence in human granulosa cells through enhancing mitophagy

   Cell biology and toxicology·13 Jan 2026

More on Cellular senescence

1. Advanced glycation end products impair blood-brain barrier in human cells.

   “Furthermore, AGE exposure disrupts blood-brain barrier (BBB) integrity and impairs amyloid-β transport in an in vitro BBB model.”

   Cellsin an in vitro BBB model

   Advanced glycation end products drive blood-brain barrier lipid dysregulation via RAGE-ABCA1 signaling to promote neurovascular dysfunction in Alzheimer's disease

   Molecular psychiatry·3 Sep 2026

1. Advanced glycation end products increase lipid-droplet in human cells.

   “In human brain endothelial cells, AGE exposure induces lipid metabolic reprogramming characterized by enhanced LD accumulation, upregulation of lipogenic machinery, and suppression of cholesterol efflux.”

   Cellsin human brain endothelial cellsbrain endothelial cell

   Advanced glycation end products drive blood-brain barrier lipid dysregulation via RAGE-ABCA1 signaling to promote neurovascular dysfunction in Alzheimer's disease

   Molecular psychiatry·3 Sep 2026

1. Advanced glycation end products activate cGAS–STING signalling in mouse cells.

   “exposure of primary microglia to AGEs induces cytosolic mtDNA release and activates cGAS-STING signaling”

   Cellsprimary microglia

   APOE4-AGE axis is linked to mtDNA release and cGAS-STING-mediated neuroinflammation in the aging brain

   Free radical biology & medicine·29 Aug 2026

More on cGAS–STING signalling

1. Advanced glycation end products induce apoptosis in human cells.

   “Concurrent treatment with high glucose and AGEs substantially suppressed SHED proliferative and migratory capacity while simultaneously enhancing apoptotic cell death and cellular senescence.”

   Cellsunder high-glucose conditions

   AGEs derived from high-sugar diets induce functional impairment of odontogenic stem cells via RAGE-mediated endoplasmic reticulum stress

   Histochemistry and cell biology·24 May 2026

More on Apoptosis

1. Advanced glycation end products decrease proliferation in human cells.

   “Concurrent treatment with high glucose and AGEs substantially suppressed SHED proliferative and migratory capacity while simultaneously enhancing apoptotic cell death and cellular senescence.”

   Cellsunder high-glucose conditions

   AGEs derived from high-sugar diets induce functional impairment of odontogenic stem cells via RAGE-mediated endoplasmic reticulum stress

   Histochemistry and cell biology·24 May 2026

1. Advanced glycation end products increase cartilage degeneration in mice.

   “AGEs aggravated cartilage degeneration, subchondral bone alterations, and chondrocyte senescence in an OA mouse model.”

   Animalsin an OA mouse model

   SIRT1 Downregulation by Advanced Glycation End Products Activates RANKL-Dependent Osteoclast Signaling and Drives Chondrocyte Senescence During Osteoarthritis Development

   Aging cell·1 May 2026

1. Advanced glycation end products decrease SIRT1 in cells.

   “SIRT1 emerged as a central regulator suppressed following AGE exposure.”

   Cellsin osteoclasts

   SIRT1 Downregulation by Advanced Glycation End Products Activates RANKL-Dependent Osteoclast Signaling and Drives Chondrocyte Senescence During Osteoarthritis Development

   Aging cell·1 May 2026

More on SIRT1

1. Advanced glycation end products inhibit mitophagy in human cells.

   “AGEs treatment significantly exacerbated hGC senescence, impaired mitochondrial function, and suppressed mitophagy in a concentration-dependent manner.”

   Cellsconcentration-dependent

   SIRT3 attenuates AGEs-induced senescence in human granulosa cells through enhancing mitophagy

   Cell biology and toxicology·13 Jan 2026

More on Mitophagy

1. Advanced glycation end products increase neurodegeneration in mouse cells.

   “Under AGE-incorporated conditions, we observed brain endothelial dysfunction and microglial activation, leading to increased neuroinflammation and neurodegeneration.”

   Cellsaged neurovascular modelAGE-anchored matrixbrain

   Extracellular matrix glycation epigenetically regulates brain aging and neurodegeneration in the in vitro aged neurovascular model

   Biomaterials·13 Jun 2025