Richard F. Loeser

This study shows that KMT2C and KMT2D regulate skeletal development through epigenetic control of chondrogenesis, with redundancy in their function during bone formation.

This study uses single-cell RNA sequencing to analyze how fibronectin fragment treatment alters chondrocyte states and transcriptional programs in primary human cells.

This study finds that female OA synovial fibroblasts show higher senescence markers and reduced oxidative stress response compared to males.

This study compares genome instability in articular chondrocytes and skin fibroblasts using whole-genome sequencing, revealing distinct mutation patterns and mutagenic mechanisms between the two cell types.

The paper identifies an adipose-complement-lipid axis that systemically regulates sensory neuron sensitization, explaining pain-structure discordance in obesity-associated osteoarthritis.

The paper identifies OA risk genes by integrating eQTLs, chromatin accessibility, and 3D chromatin structure in human chondrocytes, revealing 13 putative risk genes, 10 of which are novel.

The paper examines how 18-months of diet, exercise, or combined interventions affect the serum metabolome of knee OA patients, revealing sex-specific metabolic changes.

The paper identifies response splicing QTLs in human chondrocytes and links them to osteoarthritis risk genes through alternative splicing analysis.

This study shows that SIRT6 loss in mice leads to intervertebral disc degeneration by promoting senescence and SASP through changes in histone modifications, DNA accessibility, and autophagy.

The paper identifies 56 putative OA risk genes by integrating GWAS, chromatin structure, and RNA-seq data in chondrocytes, with SOCS2 as a novel target gene.

This study examines the transcriptional response of human chondrocytes to fibronectin fragments, finding similarities to osteoarthritis gene expression patterns.