类风湿性关节炎中破骨细胞乳酸堆积的调控机制研究进展OA

Rheumatoid arthritis(RA)is a chronic,systemic autoimmune disease that can affect multiple joints.Its core pathological features include chronic synovitis and pannus formation,ultimately leading to inflammatory destruction of articular cartilage and bone.The disease not only causes joint deformity and disability,but also triggers extra-articular complications such as cardiovascular diseases,significantly increasing mortality and severely impairing patients'quality of life.Conventional RA treatment strategies largely rely on non-steroidal anti-inflammatory drugs to control synovial tissue inflammation,often overlooking the pivotal role of osteoclasts in disease progression and their therapeutic potential.Osteoclasts serve as key effector cells mediating joint bone erosion and destruction in RA,and their metabolic reprogramming is crucial for maintaining osteoblast-osteoclast balance and regulating bone resorption.This review focuses on the shift of energy metabolism toward anaerobic oxidation in osteoclasts under pathological conditions.It systematically outlines the multiple causes of lactate accumulation resulting from anaerobic oxidation in osteoclasts,elaborates on the regulatory effects of lactate accumulation on osteoclast differentiation and bone resorption function,and further summarizes the unique advantages and application potential of targeting lactate metabolism in RA treatment.The aim is to provide a theoretical basis for the development of novel clinical therapies.