ECMremodellering

ECMremodellering refers to the dynamic turnover of the extracellular matrix (ECM) in tissues, involving coordinated degradation of existing ECM components and synthesis of new ECM. This process enables tissue development, growth, repair, and adaptation, while maintaining structural integrity.

Key players include matrix metalloproteinases (MMPs) and other proteases such as serine proteases and cathepsins, which break down collagen, elastin, and proteoglycans. Their activity is tightly regulated by inhibitors like TIMPs. Cells such as fibroblasts, osteoclasts, and chondrocytes synthesize ECM components, including collagen, elastin, and proteoglycans, and can modify ECM cross-linking through enzymes like lysyl oxidase.

Regulation of ECMremodellering involves signaling networks with transforming growth factor beta (TGF-β), platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), inflammatory cytokines, and mechanical cues from tissue stiffness and strain. Integrins mediate cell–ECM interactions that influence remodeling and cellular behavior.

Physiological remodeling occurs during embryonic development, wound healing, bone turnover, and organ maturation. Pathological remodeling is linked to fibrosis, tumor progression, atherosclerosis, osteoarthritis, and chronic obstructive pulmonary disease (COPD), often featuring imbalances between degradation and synthesis or excessive matrix deposition.

Researchers study ECMremodellering through biochemical assays of MMP activity, gene expression analyses, histology, and in vivo imaging. Therapeutic considerations aim to restore balance in remodeling, including approaches targeting MMP activity or ECM synthesis, to mitigate fibrosis, cancer progression, and related diseases.