The extracellular matrix (ECM) is a dynamic and multifunctional component of the cellular microenvironment, playing crucial roles in tissue architecture, cell differentiation, and disease. ECM dynamics involve the constant deposition, degradation, and modification of its components, which are essential for regulating cell behaviors such as proliferation, migration, and differentiation. Abnormal ECM dynamics can lead to congenital defects and pathological conditions like tissue fibrosis and cancer. Key players in ECM degradation and remodeling include metalloproteinases (MMPs), disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS), serine proteinases, and hyaluronidases. These enzymes are tightly regulated at multiple levels, from transcriptional to posttranslational control, to ensure proper ECM dynamics. The physical, biochemical, and biomechanical properties of the ECM also influence cell behaviors, including migration, anchorage, and signaling. For example, ECM elasticity can affect cell differentiation and tissue function, and cells can sense and respond to these properties by exerting forces against the ECM. In development, ECM dynamics are critical for processes such as epithelial branching morphogenesis, skeletal development, and stem cell maintenance. Abnormal ECM dynamics can result in defects in these processes, contributing to diseases like cancer and osteoporosis. Understanding the mechanisms of ECM remodeling is essential for developing therapeutic interventions and advancing tissue engineering and regenerative medicine.The extracellular matrix (ECM) is a dynamic and multifunctional component of the cellular microenvironment, playing crucial roles in tissue architecture, cell differentiation, and disease. ECM dynamics involve the constant deposition, degradation, and modification of its components, which are essential for regulating cell behaviors such as proliferation, migration, and differentiation. Abnormal ECM dynamics can lead to congenital defects and pathological conditions like tissue fibrosis and cancer. Key players in ECM degradation and remodeling include metalloproteinases (MMPs), disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS), serine proteinases, and hyaluronidases. These enzymes are tightly regulated at multiple levels, from transcriptional to posttranslational control, to ensure proper ECM dynamics. The physical, biochemical, and biomechanical properties of the ECM also influence cell behaviors, including migration, anchorage, and signaling. For example, ECM elasticity can affect cell differentiation and tissue function, and cells can sense and respond to these properties by exerting forces against the ECM. In development, ECM dynamics are critical for processes such as epithelial branching morphogenesis, skeletal development, and stem cell maintenance. Abnormal ECM dynamics can result in defects in these processes, contributing to diseases like cancer and osteoporosis. Understanding the mechanisms of ECM remodeling is essential for developing therapeutic interventions and advancing tissue engineering and regenerative medicine.