Epigallocatechin gallate (EGCG), a major polyphenolic compound in green tea, exhibits preventive and therapeutic effects in many fibrotic diseases. Tissue fibrosis is characterized by excessive deposition of collagen fibrils in the extracellular matrix, primarily due to dysregulation of cellular signaling pathways. However, we have previously demonstrated that EGCG directly inhibits the formation of collagen fibrils from collagen monomers under in vitro experimental conditions that excluded involvement of cellular signaling systems. This review explores the antifibrotic action of EGCG, which may occur through (i) its influence on cellular signaling and (ii) direct binding to collagen monomers, leading to the inhibition of pathological fibrillogenesis, as well as discuss the prospects for targeting the collagen assembly process.
Tarahovsky et al. (Sun,) studied this question.
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