ECMansamling

ECM accumulation, known in Swedish medical literature as ECM-ansamling, refers to the excessive deposition of components of the extracellular matrix (ECM) within tissues. The ECM comprises proteins such as collagens, elastin, fibronectin, laminins, and proteoglycans that provide structural support and influence cell behavior. When accumulation occurs, tissue architecture can become distorted and mechanical properties such as stiffness increase.

The process typically follows chronic injury or ongoing inflammatory stimuli. Persistent activation of resident fibroblasts and conversion to myofibroblasts leads to increased synthesis of matrix proteins. Degradation of the ECM may be reduced due to altered activity of metalloproteinases and their inhibitors (MMPs and TIMPs). Enzymatic cross-linking, for example by lysyl oxidase, further stabilizes the deposited matrix and contributes to tissue stiffening.

ECM accumulation is a central feature of fibrotic diseases in multiple organs. Common examples include liver fibrosis and cirrhosis, pulmonary fibrosis, renal fibrosis, and skin involvement in scleroderma. The resulting changes in tissue mechanics and architecture can impair organ function and promote a cycle of ongoing injury.

Diagnosis relies on a combination of clinical assessment, imaging to evaluate fibrotic changes, and, when appropriate, histological biopsy. Noninvasive biomarkers and elastography techniques are increasingly used to stage fibrosis and monitor progression.

Treatment emphasizes addressing the underlying cause of injury and, where available, antifibrotic therapies that slow progression or reduce ECM deposition. Approaches in development target pathways such as TGF-β signaling, MMP/TIMP balance, and cross-linking enzymes, with organ- and disease-specific considerations.

See also: extracellular matrix, fibrosis, tissue remodeling, myofibroblast.