Premium
Abrogation of the fibrotic effect of transforming growth factor‐β in dermal wound healing
Author(s) -
Parrelli Jo M.,
Meisler Natalie,
Cutroneo Kenneth R.
Publication year - 1997
Publication title -
wound repair and regeneration
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.847
H-Index - 109
eISSN - 1524-475X
pISSN - 1067-1927
DOI - 10.1046/j.1524-475x.1997.50204.x
Subject(s) - extracellular matrix , transforming growth factor , wound healing , growth factor , fibrosis , transforming growth factor beta , glucocorticoid , cancer research , transforming growth factor, beta 3 , microbiology and biotechnology , chemistry , endocrinology , medicine , immunology , biology , tgf alpha , receptor
The growth factor, transforming growth factor‐β1, which under normal circumstances promotes wound healing by stimulating local fibroblasts to produce collagen and other extracellular matrix proteins, has also been implicated as the primary causative agent of fibrosis. Because transforming growth factor‐β1 is capable of stimulating its own production by fibroblasts, its normally beneficial effects may become amplified to the point where excess extracellular matrix accumulation occurs, thereby causing abnormal scarring. Therefore, strategies that block or counter the effects of transforming growth factor‐β1 may be useful in preventing or decreasing fibrosis. One such strategy is the use of glucocorticoid steroids such as dexamethasone, which normally have the opposite effect of transforming growth factor‐β1, namely the impairment of wound healing. When used in conjunction with transforming growth factor‐β1, glucocorticoid steroids may normalize the effect of transforming growth factor‐β1 on collagen synthesis, thereby reducing excessive collagen deposition and fibrosis.