Glucose involvement in articular cartilage remodeling

Currently, the interest in studying glucose as a signaling molecule and a regulator of chondrocyte metabolism is increasing significantly. There is little available data on chondrocytes’ ability to respond to extracellular glucose concentration changes that help them to avoid harmful effects resulting from the lack or accumulation of intracellular glucose. We have collected and analyzed the information about the mechanism of glucose influence on articular cartilage chondrocyte in this study. We have learned that chondrocytes adapt to both high and low glucose concentrations by modulating the synthesis and degradation of GluT1. Consequently, glucose in different concentrations affects many fundamental cellular functions such as the cartilage matrix synthesis and disruption, proliferation, differentiation, and apoptosis. To build a functional model of glucose participation in articular cartilage remodeling the exhaustive search and analysis of literature has been performed using open access resources. The scheme reflects key processes that have direct or indirect effects on the catabolic or anabolic function of chondrocytes. As a result, we have created a functional model that shows the effect of glucose on the suppression or expression of compounds that are actively involved in cartilage tissue remodeling. For example, these are compounds such as nitric oxide, aggrecans and type II collagen and others. Despite the role of glucose in energy metabolism in all cell types, including chondrocytes, high concentrations of glucose can also have a harmful effect. The advantage of this model is systematic data, which facilitates the perception of the results and their relevance.