Jana Riegger

This study identifies mitochondrial dysfunction and impaired osteogenic capacity as key features of stress-induced osteoblast senescence using in vitro models and transcriptomic analysis.

This study identifies GDF-15 as a stress-responsive cytokine upregulated in PTOA, which promotes a pro-regenerative response in chondrocytes after cartilage injury.

The paper shows mechanical stress reprograms chondrocytes into mechano-activated chondroprogenitors (MACs) that drive cartilage repair, which is arrested in osteoarthritis.

Senolytic therapy with Dasatinib and Quercetin improves chondrocyte function in osteoarthritis by reducing senescence-associated secretory phenotype factors and increasing anabolic gene expression.