ECM-receptor interaction pathway (ECM-RI)

The ECM-receptor interaction pathway is a fundamental biological process involving the binding of extracellular matrix (ECM) components to specific cell surface receptors (Source: KEGG hsa04512). This pathway is composed of various structural proteins, such as collagens, laminins, and fibronectins, which interact with transmembrane receptors like integrins, CD44, and proteoglycans (Source: StatPearls, NBK535444). These interactions are essential for maintaining the structural integrity of tissues and for transducing external mechanical and chemical signals into the cell to regulate survival, proliferation, and motility. In pathological states, such as cancer, the pathway is often hijacked to promote tumor cell invasion and metastasis through remodeled ECM and altered receptor expression (Source: PMID: 30634152). Pharmacological targeting of this pathway typically involves small molecules or monoclonal antibodies directed at specific receptors, most notably integrins, to treat conditions ranging from thrombotic disorders to autoimmune diseases and malignancies (Source: PMID: 28974151). By disrupting these interactions, drugs can effectively inhibit pathological cell adhesion and signaling, though this often comes with risks such as impaired wound healing or bleeding (Source: PMID: 11030310).

Other names

Extracellular matrix-receptor interactionKEGG hsa04512ECM-receptor interaction

Drugs targeting this pathway primarily act as antagonists to transmembrane receptors, such as integrins, preventing their binding to extracellular matrix ligands like fibrinogen, fibronectin, or vascular cell adhesion molecule-1 (VCAM-1). This blockade inhibits cell-to-cell or cell-to-matrix adhesion and disrupts downstream signaling pathways (e.g., FAK, Src, and PI3K/Akt) that are essential for platelet aggregation, leukocyte extravasation, or tumor cell survival and migration (Source: PMID: 28974151, PMID: 24655083).