Glycolysis is an emerging regulator of osteoarthritis (OA). OA is a leading cause of disability in the elderly, with limited effective therapeutic approaches due to unclear pathogenesis. As OA progresses, cellular metabolism and energy production change, and metabolic reprogramming highlights the importance of specific metabolic pathways in disease progression. Glycolysis, a crucial part of glucose metabolism, bridges metabolic and inflammatory dysfunctions. The glycolytic pathway is involved in various areas of metabolism and inflammation and is associated with various transcription factors. It remains unclear whether changes in the glycolytic pathway and its key enzymes are linked to OA onset or progression. This review summarizes the role of glycolysis in mediating cellular metabolic reprogramming in OA and its role in inducing tissue inflammation and injury, aiming to provide insights into its pathological functions and propose new treatment targets for OA. OA is characterized by pathological changes in joint structure, including cartilage degeneration, synovial inflammation, and subchondral sclerosis with osteophyte formation. Articular cartilage is a reduced cellular, avascular, neurogenic, and lymphoid tissue with limited oxygen and glucose availability. Chondrocytes, the only cells present in articular cartilage, are the primary controllers of cartilage tissue metabolism. Articular hyaline cartilage consists of chondrocytes within the extracellular matrix (ECM), which is generated and maintained by chondrocytes. The subchondral bone, synovium, and joint capsule have a direct vascular supply. Inflammation of the synovium, massive destruction of articular cartilage, and persistent joint destruction accompanied by severe joint pain are the most predominant pathologic features of OA. Recent studies have found that changes in glycolysis (including glycolysis, pentose phosphate pathway, and tricarboxylic acid cycle) are a new perspective on the pathogenesis of OA. Several studies have found that anaerobic and aerobic glycolysis (Warburg effect) coexist in chondrocytes of normal articular cartilage. The Warburg effect is also a characteristic of some arthritic diseases. Warburg effect means that under sufficient oxygen conditions, glycolytic metabolism is still needed to provide sufficient energy for cell proliferation. This process involves many enzymes, such as pyruvate kinase M2 (PKM2), lactate dehydrogenase A (LDHA), hexokinase2 (HK2), and 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), and related studies have shown that the increase of these enzymes in OA chondrocytes can promote the occurrence of inflammatory reaction, apoptosis of chondrocytes, and other pathological changes. A significant relationship between the progression of OA and glycolysis has been further demonstrated, as levels of abnormal products ofGlycolysis is an emerging regulator of osteoarthritis (OA). OA is a leading cause of disability in the elderly, with limited effective therapeutic approaches due to unclear pathogenesis. As OA progresses, cellular metabolism and energy production change, and metabolic reprogramming highlights the importance of specific metabolic pathways in disease progression. Glycolysis, a crucial part of glucose metabolism, bridges metabolic and inflammatory dysfunctions. The glycolytic pathway is involved in various areas of metabolism and inflammation and is associated with various transcription factors. It remains unclear whether changes in the glycolytic pathway and its key enzymes are linked to OA onset or progression. This review summarizes the role of glycolysis in mediating cellular metabolic reprogramming in OA and its role in inducing tissue inflammation and injury, aiming to provide insights into its pathological functions and propose new treatment targets for OA. OA is characterized by pathological changes in joint structure, including cartilage degeneration, synovial inflammation, and subchondral sclerosis with osteophyte formation. Articular cartilage is a reduced cellular, avascular, neurogenic, and lymphoid tissue with limited oxygen and glucose availability. Chondrocytes, the only cells present in articular cartilage, are the primary controllers of cartilage tissue metabolism. Articular hyaline cartilage consists of chondrocytes within the extracellular matrix (ECM), which is generated and maintained by chondrocytes. The subchondral bone, synovium, and joint capsule have a direct vascular supply. Inflammation of the synovium, massive destruction of articular cartilage, and persistent joint destruction accompanied by severe joint pain are the most predominant pathologic features of OA. Recent studies have found that changes in glycolysis (including glycolysis, pentose phosphate pathway, and tricarboxylic acid cycle) are a new perspective on the pathogenesis of OA. Several studies have found that anaerobic and aerobic glycolysis (Warburg effect) coexist in chondrocytes of normal articular cartilage. The Warburg effect is also a characteristic of some arthritic diseases. Warburg effect means that under sufficient oxygen conditions, glycolytic metabolism is still needed to provide sufficient energy for cell proliferation. This process involves many enzymes, such as pyruvate kinase M2 (PKM2), lactate dehydrogenase A (LDHA), hexokinase2 (HK2), and 6-phosphofructo-2-kinase/fructose-2,6-biphosphatase 3 (PFKFB3), and related studies have shown that the increase of these enzymes in OA chondrocytes can promote the occurrence of inflammatory reaction, apoptosis of chondrocytes, and other pathological changes. A significant relationship between the progression of OA and glycolysis has been further demonstrated, as levels of abnormal products of