The action of transforming-growth-factor (TGF)-beta following inflammatory responses
is characterized by increased production of extracellular matrix (ECM) components,
as well as mesenchymal cell proliferation, migration, and accumulation. Thus, TGF-beta
is important for the induction of fibrosis often associated with chronic phases of
inflammatory diseases. This common feature of TGF-related pathologies is observed
in many different organs. Therefore, in addition to the description of the common
TGF-beta-pathway, this review focuses on TGF-beta-related pathogenetic effects in
different pathologies/organs, i. e., arthritis, diabetic nephropathy, colitis/Crohn's
disease, radiation-induced fibrosis, and myocarditis (including their similarities
and dissimilarities). However, TGF-beta exhibits both exacerbating and ameliorating
features, depending on the phase of disease and the site of action. Due to its central
role in severe fibrotic diseases, TGF-beta nevertheless remains an attractive therapeutic
target, if targeted locally and during the fibrotic phase of disease.