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Fibroblasts are the principal cells of connective tissue, responsible for secreting and organizing the extracellular matrix (ECM), which consists of proteins such as collagen, elastin, and proteoglycans (Wynn, 2008, J. Clin. Invest. [1]). This system provides the essential structural scaffold for organs and plays a critical role in wound healing and tissue homeostasis (Alberts et al., 2002, Molecular Biology of the Cell [2]). In various diseases, fibroblasts undergo pathological activation into myofibroblasts, leading to the excessive accumulation of ECM, a process known as fibrosis that can result in organ failure (Richeldi et al., 2014, N. Engl. J. Med. [3]). In oncology, the fibroblast-rich stroma or tumor microenvironment acts as a physical and biochemical barrier that promotes tumor growth and hinders the penetration of chemotherapeutic agents (Sahai et al., 2020, Nat. Rev. Cancer [4]). Therapeutic strategies targeting this system involve modulating signaling pathways like TGF-beta or directly degrading matrix components to restore normal tissue architecture and improve drug delivery (Henderson et al., 2013, Nature [5]).
Inhibition of fibroblast proliferation and activation via tyrosine kinase or TGF-beta signaling pathways, and enzymatic degradation of extracellular matrix components like collagen.
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