PRMT1 mediates RANKL-induced osteoclastogenesis and contributes to bone loss in ovariectomized mice

Osteoporosis: protein trigger for postmenopausal bone loss identified A protein that helps trigger bone loss in postmenopausal osteoporosis could be a potential therapeutic target. After the menopause, decreases in estrogen hormone levels can lead to bone diseases including osteoporosis. Osteoporosis occurs when the bone remodeling process breaks down, and bone resorption by cells called osteoclasts outweighs bone formation. In a mouse model of postmenopausal osteoporosis, Jong-Hwan Park at Chonnam National University, Gwangju, South Korea and co-workers identified key players in the progression of the disease. The team focused on factors influencing the RANKL protein, a known controller of bone remodeling. They found that RANKL triggers the formation of osteoclasts via interaction with another protein, PRMT1. Suppression of PRMT1 by estrogen appears to inhibit excessive osteoclast formation, suggesting it could be a potential therapeutic target for treating osteoporosis.