Fibroblast cell (FB)

Fibroblasts are the most common cells of connective tissue, responsible for the synthesis of the extracellular matrix (ECM) and collagen, which provide the structural framework for tissues (NIH, 2024). They play a vital role in wound healing and tissue repair by migrating to sites of injury and differentiating into contractile myofibroblasts (StatPearls, 2023). In pathological states, dysregulated fibroblast activity is a primary driver of fibrosis in organs such as the lungs, liver, and kidneys, where excessive ECM deposition leads to organ failure (Journal of Clinical Investigation, 2022). Additionally, in the tumor microenvironment, cancer-associated fibroblasts (CAFs) actively promote tumor progression, metastasis, and resistance to chemotherapy (Nature Reviews Cancer, 2021). Therapeutically, fibroblast cells are targeted not as a single molecule, but through specific signaling pathways and surface proteins expressed during their activation. Common pharmacological strategies involve the inhibition of tyrosine kinase receptors such as FGFR, PDGFR, and VEGFR, or the modulation of the TGF-β signaling pathway to prevent the transition of quiescent fibroblasts into pathological myofibroblasts (Nature Reviews Drug Discovery, 2023). Drugs like nintedanib and pirfenidone are clinical examples of therapies used to slow the progression of fibrotic diseases by modulating these fibroblast-driven processes (FDA, 2014). Recent advancements also include the development of CAR-T cells and radioligands targeting the Fibroblast Activation Protein (FAP) to specifically deplete activated fibroblast populations in cancer and chronic inflammation (PubMed, 2024).

Other names

Connective tissue cellMyofibroblastCancer-associated fibroblastCAFStromal cell

Modulation of fibroblast activity through the inhibition of profibrotic signaling (TGF-beta, PDGF, FGF), inhibition of extracellular matrix cross-linking (e.g., LOXL2), or targeted depletion of activated subsets via cell-surface proteases like FAP.