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The extracellular matrix (ECM) structural components represent a diverse and complex network of extracellular macromolecules, including collagens, elastins, fibronectins, laminins, and proteoglycans, that provide the essential physical scaffolding for all tissues and organs (Frantz et al., 2010). Beyond its role as a passive structural support, the ECM is a dynamic environment that actively regulates cell behavior—such as survival, proliferation, and differentiation—through biochemical and biomechanical signaling (Hynes & Naba, 2012). In many diseases, the ECM undergoes pathological remodeling; for instance, excessive deposition of collagen leads to fibrosis in the liver, lungs, and heart, while degradation of the matrix is a hallmark of osteoarthritis and cancer metastasis (Wynn, 2008; Nallanthighal et al., 2019). Therapeutic strategies targeting the ECM include the use of enzymes like collagenase and hyaluronidase to break down excessive matrix, as well as small molecules like pirfenidone that inhibit the synthesis of new matrix components. However, because the ECM is fundamental to the integrity of nearly every tissue, pharmacological interventions must carefully balance the reduction of pathological matrix with the preservation of normal physiological structure and function.
Enzymatic degradation of matrix components, inhibition of fibroblast-mediated matrix synthesis, and disruption of matrix-cell signaling pathways.
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