Molecular roles in membrane receptor signaling pathways and cascade reactions in chondrocytes: a review

Abstract

Articular cartilage (AC) is a specialized connective tissue with unique biological and mechanical properties, which depends on the biological effects of each resident chondrocyte and its surrounding extracellular matrix (ECM) to form a unit that operates in a constant and balanced feedback loop. The surface membrane receptors of chondrocytes play a crucial role in the feedback balance of this biological unit. Various biological signals outside chondrocytes, such as water-soluble chemical signal molecules and mechanical signals, are unable to directly enter the cell and must first bind to the plasma membrane receptors to induce changes in the level and activity of intracellular signal transduction molecules. These changes then transmit through signaling cascade pathways into the nucleus, changing the cell phenotype, and producing physiological or pathological changes. Specific chemical and mechanical signals break the feedback balance of cartilage tissue units through membrane receptors. In the ECM environment, the molecular actions of chondrocyte membrane receptors in response to these specific signals, along with associated ion channel receptors, collectively regulate the biological effects of chondrocytes. This leads to decreased chondrocyte survival and an imbalance in ECM regulation, ultimately disrupting the tissue's molecular framework and physiological feedback mechanisms, and resulting in pathological changes in cartilage tissue. To provide insights into addressing the complexities associated with cartilage tissue injury and repair engineering, this review provides a comprehensive overview of the molecular mechanisms and biological implications of chondrocyte membrane receptor-mediated signal transduction, including G protein-coupled receptors (GPCRs), enzyme-linked receptors (tyrosine kinase receptors (TKRs)), and integrin receptors.

Keywords: Chondrocytes; GPCR; Integrin; Signaling pathway; TKR.