Response eQTLs, chromatin accessibility, and 3D chromatin structure in chondrocytes provide mechanistic insight into osteoarthritis risk.

Osteoarthritis (OA) poses a significant healthcare burden with limited treatment options. While genome-wide association studies (GWASs) have identified over 100 OA-associated loci, translating these findings into therapeutic targets remains challenging. To address this gap, we mapped gene expression, chromatin accessibility, and 3D chromatin structure in primary human articular chondrocytes in both resting and OA-mimicking conditions.

The metabolome of male and female individuals with knee osteoarthritis is influenced by 18-months of weight loss intervention: the IDEA trial.

Background: The Intensive Diet and Exercise for Arthritis (IDEA) trial was a randomized trial conducted to evaluate the effects of diet and exercise on osteoarthritis (OA), the most prevalent form of arthritis. Various risk factors, including obesity and sex, contribute to OA's debilitating nature. While diet and exercise are known to improve OA symptoms, cellular and molecular mechanisms underlying these interventions, as well as effects of participant sex, remain elusive.

Response splicing QTLs in primary human chondrocytes identifies putative osteoarthritis risk genes.

Osteoarthritis affects millions worldwide, yet effective treatments remain elusive due to poorly understood molecular mechanisms. While genome-wide association studies (GWAS) have identified over 100 OA-associated loci, identifying the genes impacted at each locus remains challenging. Several studies have mapped expression quantitative trait loci (eQTL) in chondrocytes and colocalized them with OA GWAS variants to identify putative OA risk genes; however, the degree to which genetic variants influence OA risk via alternative splicing has not been explored.

A novel small molecule screening assay using normal human chondrocytes toward osteoarthritis drug discovery.

Osteoarthritis (OA) is the most common form of arthritis and a leading cause of pain and disability in adults. A central feature is progressive cartilage degradation and matrix fragment formation driven by the excessive production of matrix metalloproteinases (MMPs), such as MMP-13, by articular chondrocytes. Inflammatory factors, including interleukin 6 (IL-6), are secreted into the joint by synovial fibroblasts, and can contribute to pain and inflammation.