Our research focuses on CD5L, a critical protein regulating chondrocyte apoptosis and cartilage homeostasis in osteoarthritis. We are investigating its mechanistic role in driving cellular degradation pathways and extracellular matrix disruption, which accelerates joint deterioration.
Long-term objective:
Leverage CRISPR-based gene editing to precisely target inflammatory signaling within synovial tissues. By modulating key molecular triggers, we aim to develop therapies that prevent cartilage destruction and halt disease progression in osteoarthritis patients.
Osteoarthritis (OA), a chronic joint disease, is characterized by the systemic dysfunction and degradation of articular cartilage. OA is a leading cause of impaired mobility in the elderly and constitutes a considerable economic and societal burden in Europe, with its aging population. The total economic impact of OA ranges from 1 to 2.5% of gross national product in countries with established market economies.OA affects more than 12% of the general population and the majority of elderly people in Norway, making it one of the most frequent chronic diseases and the single most frequent cause of disability in older adults. By 2050, one in three people worldwide will suffer from OA, a disease for which we still have no cure.
OA is driven by two major interconnected processes: local inflammation and joint degradation. Chondrocytes, the primary specialized cells within the joint, play a crucial role in these processes. The apoptosis of chondrocytes is a key pathogenic mechanism leading to cartilage degradation in OA. The presence of fewer living chondrocytes leads to lower levels of extracellular matrix protein secretion, exacerbating cartilage erosion and driving inflammation. The molecular mechanisms driving chondrocyte metabolism, apoptosis and inflammation are still poorly understood. Current therapeutic options for patients are limited to pain management, with joint replacement surgery in cases of severe symptoms. There is, therefore, an urgent need to identify new therapeutic targets and to develop innovative treatments to halt the progression of OA.