Growth factors, such as transforming growth factor-beta (TGF-β), platelet-derived growth factor (PDGF), and fibroblast growth factors (FGFs), play critical roles in tissue repair, regeneration, and fibrosis. Their involvement in the pathogenesis of fibrotic diseases is well-documented, as they regulate fibroblast proliferation, differentiation, and extracellular matrix production. However, rather than being used to treat fibrosis directly, growth factors are often targets for anti-fibrotic therapies. Excessive activity of certain growth factors, particularly TGF-β, is a major driver of fibrosis in organs like the liver, lungs, and kidneys.

Experimental and some early clinical studies have explored the therapeutic modulation (not supplementation) of growth factors to control fibrotic processes. For example, inhibitors of TGF-β signaling are being tested as potential anti-fibrotic agents in diseases such as idiopathic pulmonary fibrosis and systemic sclerosis. Conversely, some growth factors (e.g., hepatocyte growth factor, HGF) have demonstrated anti-fibrotic properties in animal models by counteracting the effects of pro-fibrotic growth factors.

In summary, while the scientific community acknowledges the centrality of growth factors in fibrosis biology, clinical use of exogenous growth factors to treat fibrosis is not established and may be detrimental. Instead, therapies typically aim to inhibit or modulate growth factor pathways to reduce fibrosis. The evidence base for such approaches is growing, with several agents in preclinical or early clinical development, but routine clinical application is not yet standard.