Extracellular matrix and cell-surface components (ECM)

The extracellular matrix (ECM) and cell-surface components constitute a complex scaffolding of extracellular macromolecules, such as collagen, enzymes, and glycoproteins, that provide structural and biochemical support to surrounding cells (Yue, 2014). This term is a broad classification rather than a single target, encompassing the 'matrisome' which includes hundreds of distinct proteins that regulate cell behavior, signaling, and tissue homeostasis (Naba et al., 2012). In diseases like cancer, the ECM is often remodeled to promote tumor growth and metastasis, while in fibrotic diseases, excessive ECM deposition leads to organ dysfunction (Walker et al., 2018). Therapeutic strategies targeting this system include the use of monoclonal antibodies against cell-surface integrins or enzymes that modify the matrix environment to improve drug delivery or inhibit pathological signaling (Theocharis et al., 2016). For example, integrin antagonists are used in cardiovascular and inflammatory diseases to prevent cell adhesion and migration. Additionally, enzymes like hyaluronidase are employed to degrade matrix components and enhance the dispersion of co-administered drugs. However, because these components are ubiquitous throughout the body, achieving high selectivity remains a significant challenge in drug development. Safety concerns often involve the disruption of normal tissue architecture or impaired wound healing processes. Consequently, drug discovery efforts usually focus on specific isoforms or disease-specific modifications within the matrix rather than the entire system. Overall, the ECM is a dynamic environment that serves as both a physical barrier and a signaling hub in human physiology.

Other names

Extracellular matrixCell-surface proteinsMatrisomeIntercellular matrixCell-matrix components

Modulation of cell-matrix interactions, inhibition of cell-surface adhesion receptors (e.g., integrin antagonism), or enzymatic degradation of matrix components (Theocharis et al., 2016).